erythromycin reference
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(erythromycin · DailyMed)
Registered Malawi · PMRA

ALISERYL WS COMBINATION PRODUCT POWDER FOR RECONSTITUTION

ERYTHROMYCIN THIOCYANATE, OXYTETRACYCLINE HCL, STREPTOMYCIN SULFATE & COLISTIN SULFATE

PMPB/PL524/1 POWDER FOR RECONSTITUTION alimentary tract and metabolism INN generic

What it does

Colistin is an antibiotic used to treat serious infections caused by certain bacteria, especially when other antibiotics are not effective.

Commonly used for: serious bacterial infections, pneumonia, blood infections (sepsis)

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/PL524/1
Registration date
27/11/2020
Expiry date
30/06/2021
Status
Registered
Active ingredient
ERYTHROMYCIN THIOCYANATE, OXYTETRACYCLINE HCL, STREPTOMYCIN SULFATE & COLISTIN SULFATE
Strength
-
Pack size
-
Therapeutic class
-
ATC class (WHO)
A07AA - Antibiotics
RxNorm RxCUI
2709
Manufacturer / MAH
-
Applicant / LTR
-
Country of origin
-

Source: Pharmacy and Medicines Regulatory Authority · fetched 2026-04-21 17:37:45 · updated 2026-09-22 04:33:04

Drug Interactions

165
Check interactions

Pharmacodynamic Warnings

Oxytetracycline appears in TABLE 1: Drugs that cause hepatotoxicity

Streptomycin appears in TABLE 2: Drugs that cause nephrotoxicity

Erythromycin appears in TABLE 9: Drugs that prolong the QT interval

Streptomycin appears in TABLE 19: Drugs that cause ototoxicity

Streptomycin appears in TABLE 20: Drugs with neuromuscular blocking effects

Severe (17)

Agalsidasealfa - decreases effects

Aminoglycosidesarepredictedtodecreasetheeffectsof agalsidasealfa.Avoid.oTheoretical

Severe Theoretical

Agalsidasebeta - decreases effects

Aminoglycosidesarepredictedtodecreasetheeffectsof agalsidasebeta.Avoid.oTheoretical

Severe Theoretical

Antipsychotics, Second Generation - increases exposure

Erythromycin is predicted to increase the exposure to antipsychotics, second generation (cariprazine). Avoid.

Severe Study

Cariprazine - increases exposure

Erythromycin is predicted to increase the exposure to antipsychotics, second generation (cariprazine). Avoid.

Severe Study

Eletriptan - increases exposure

Erythromycin moderately increases the exposure to triptans (eletriptan). Avoid.

Severe Study

Moderate (41)

Alfentanil - increases exposure

Erythromycinispredictedtoincreasetheexposuretoopioids (alfentanil,buprenorphine,fentanyl,oxycodone).Monitorand adjustdose.oStudy com/codemedicalapps/ cal Applications)

Moderate Study

Amlodipine - increases exposure

Erythromycin is predicted to increase the exposure to calcium channel blockers (amlodipine, felodipine, lacidipine, lercanidipine, nicardipine, nifedipine, nimodipine). Monitor and adjust dose.

Moderate Study

Antiarrhythmics - increases exposure

Erythromycin is predicted to increase the exposure to antiarrhythmics (propafenone). Monitor and adjust dose.

Moderate Study

Antiepileptics - increases concentration

Erythromycin markedly increases the concentration of antiepileptics (carbamazepine). Monitor concentration and adjust dose.

Moderate Study

Atorvastatin - increases exposure

Erythromycins slightly increases the exposure to statins (atorvastatin). Monitor and adjust dose.

Moderate Study

Unknown (107)

Abemaciclib - increases exposure

Erythromycin is predicted to increase the exposure to abemaciclib.

Unknown Study

Acalabrutinib - increases exposure

Erythromycin is predicted to increase the exposure to acalabrutinib. Avoid or monitor.

Unknown Study

Afatinib - increases exposure

Macrolides are predicted to increase the exposure to afatinib.

Unknown Study

Alphablockers - increases exposure

Erythromycin is predicted to increase the exposure to alpha blockers (tamsulosin).

Unknown Theoretical

Alprazolam - increases exposure

Erythromycin is predicted to increase the exposure to benzodiazepines (alprazolam).

Unknown Study

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

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

About colistin

Colistin is an antibiotic used to treat serious infections caused by certain bacteria, especially when other antibiotics are not effective.

What it treats

  • serious bacterial infections
  • pneumonia
  • blood infections (sepsis)

How it works

Colistin works by attacking the outer membrane of bacteria, leading to their death and helping to clear the infection.

Who it's for

This medicine is for adults and children with severe infections caused by bacteria that are resistant to other treatments.

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

About erythromycin

Erythromycin is an antibiotic used to treat various bacterial infections.

What it treats

  • bacterial infections
  • bronchitis
  • pneumonia
  • skin infections
  • ear infections

How it works

It works by stopping the growth of bacteria, helping the body to fight off infections.

Who it's for

It is suitable for adults and children who have certain bacterial infections.

Drug class

Macrolides

Cautions

  • • Be careful if you are taking other medications that can affect heart rhythm.

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

About oxytetracycline

Oxytetracycline is an antibiotic used to treat various bacterial infections.

What it treats

  • bacterial infections
  • acne
  • respiratory infections
  • urinary tract infections

How it works

It works by stopping the growth of bacteria, helping to eliminate the infection.

Who it's for

It is for adults and children over the age of 12 who have specific bacterial infections.

Drug class

Tetracyclines

Cautions

  • • Avoid use with other medications that can harm the liver.

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

About streptomycin

Streptomycin is an antibiotic used to treat various bacterial infections.

What it treats

  • tuberculosis (TB)
  • bacterial infections
  • plague

How it works

Streptomycin works by stopping the growth of bacteria, helping the body fight off the infection.

Who it's for

This medication is for people diagnosed with certain bacterial infections, particularly those resistant to other antibiotics.

Drug class

Aminoglycosides

Cautions

  • • Be careful if you are taking other medications that can harm the kidneys.
  • • Avoid using with drugs that can affect hearing.
  • • Use caution if you are on medications that can relax muscles.

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

About thiocyanate

Thiocyanate is a compound that can affect the body in various ways, often related to its role in certain medical conditions.

What it treats

  • used in some medical tests
  • helps assess thyroid function

How it works

Thiocyanate can influence how the body uses iodine, which is important for making thyroid hormones.

Who it's for

Thiocyanate may be used for individuals undergoing tests for thyroid-related issues.

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

Clinical monograph: Oxytetracycline

BNF-referenced

Oxytetracycline is a broad-spectrum antibiotic belonging to the tetracycline class. It is effective against a variety of bacterial infections, including those caused by Chlamydia, Rickettsia, and Mycoplasma. This medication works by inhibiting protein synthesis in bacteria, making it a vital option in treating susceptible infections. Its use is cautioned in pediatric populations due to potential adverse effects on bone and dental development.

Indications

  • Bacterial infections (e.g. Chlamydia, Rickettsia, Mycoplasma)
  • Acne
  • Prophylaxis of asymptomatic meningococcal carrier state (not recommended)

Dosage

Adults: For adult patients, the typical dosage of oxytetracycline for susceptible infections is 100 mg twice daily for 5 days. For other conditions, such as acne, the dosage may be 500 mg twice daily, usually for a duration of 6 to 12 weeks, with the possibility of repeating the course intermittently.

Mechanism of action

Oxytetracycline exerts its antibacterial effects by binding to the 30S ribosomal subunit of bacteria, inhibiting the binding of aminoacyl-tRNA to the mRNA-ribosome complex. This action prevents the synthesis of proteins essential for bacterial growth and replication, leading to the bacteriostatic effect of the drug.

Pharmacodynamics

The pharmacodynamics of oxytetracycline involve its ability to inhibit bacterial protein synthesis, which is critical for the growth and reproduction of bacteria. The drug demonstrates a broad spectrum of activity against both Gram-positive and Gram-negative organisms, as well as some atypical pathogens. Its effectiveness can be influenced by the presence of tetracycline resistance mechanisms in certain bacterial strains.

Pharmacokinetics

Oxytetracycline is well absorbed from the gastrointestinal tract, with peak plasma concentrations occurring approximately 1-2 hours after oral administration. It has a relatively long half-life of about 8-10 hours, allowing for twice-daily dosing. The drug is widely distributed in body tissues and fluids, including the liver, kidneys, and lungs, but is less effective in central nervous system infections due to limited penetration. It is primarily excreted via urine, and dosage adjustments may be necessary in patients with renal impairment.

Contra-indications

  • Children under 12 years due to deposition in growing bone and teeth, causing staining and occasionally dental hypoplasia

Adverse effects

  • Gastrointestinal disturbances
  • Photosensitivity
  • Dental discoloration
  • Hepatotoxicity
  • Renal impairment
  • Skin reactions including rash and urticaria
  • Ataxia
  • Hearing impairment
  • Colitis
  • Systemic lupus erythematosus exacerbation

Interactions

  • Antacids and supplements containing calcium, magnesium, or iron may reduce absorption
  • Oral contraceptives may be less effective
  • Other tetracyclines
  • Warfarin (may increase anticoagulant effect)

Precautions

  • Use with caution in patients with renal impairment
  • Monitor for hepatic toxicity in long-term use
  • Patients should be advised to avoid excessive sunlight exposure
  • Discontinue if systemic lupus erythematosus develops or worsens

Pregnancy

Oxytetracycline is contraindicated during pregnancy due to potential harm to fetal development, particularly affecting bone and dental health.

Breast-feeding

Use with caution; oxytetracycline is excreted in breast milk and may affect the infant's dental health.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Formulations

  • Oxytetracycline 250 mg tablets
  • Oxytetracycline oral suspension
  • Oxytetracycline oral solution
BNF 85 (British National Formulary) p.646 BNF for Children 2019-2020 p.389 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: Streptomycin

BNF-referenced

Streptomycin is an aminoglycoside antibiotic that exhibits bactericidal activity against a variety of gram-negative and some gram-positive bacteria. It is primarily used in the treatment of tuberculosis, particularly strains resistant to other treatments, and is also effective against specific infections caused by Yersinia pestis and Brucella species. Due to its potential for toxicity, including nephrotoxicity and ototoxicity, careful monitoring during therapy is essential.

Indications

  • Tuberculosis, resistant to other treatment
  • Brucellosis (as an adjunct to doxycycline)
  • Severe gram-negative infections (specific cases)

Dosage

Adults: For tuberculosis: 15 mg/kg daily (maximum 1 g per dose), reduce in those under 50 kg and over 40 years. For other infections: 3 mg/kg daily in 3 divided doses, increased if necessary up

Mechanism of action

Streptomycin enters bacterial cells through a three-phase process. Initially, it binds electrostatically to negatively charged components of bacterial cell membranes, increasing permeability and allowing entry. This is followed by energy-dependent transport into the cytoplasm where it binds to the 30S ribosomal subunit, causing mistranslation of proteins and disrupting membrane integrity. The resultant damage leads to concentration-dependent bactericidal effects, including immediate and delayed actions due to impaired protein synthesis.

Pharmacodynamics

Streptomycin has a narrow spectrum of activity, effective against susceptible strains of Yersinia pestis, Francisella tularensis, Brucella, and certain strains of gram-negative bacilli and gram-positive cocci. Resistance has reduced its effectiveness against many pathogens, and it is not effective against Pseudomonas aeruginosa. The drug's therapeutic index is narrow, necessitating close monitoring for toxic effects, particularly nephrotoxicity and ototoxicity.

Pharmacokinetics

Streptomycin is administered parenterally due to poor oral absorption. After intramuscular injection, it achieves peak plasma concentrations within 1-2 hours. It is distributed widely in body tissues and fluids, but does not penetrate well into the central nervous system. The drug is primarily eliminated unchanged by the kidneys, necessitating dosage adjustments in renal impairment. The half-life is approximately 2-3 hours in individuals with normal renal function.

Contra-indications

  • Hypersensitivity to streptomycin or other aminoglycosides
  • Myasthenia gravis (due to risk of neuromuscular blockade)
  • Pregnancy (especially in the second and third trimesters due to risk of auditory or vestibular nerve damage)

Adverse effects

  • Nephrotoxicity
  • Ototoxicity
  • Nausea
  • Vomiting
  • Diarrhea
  • Electrolyte imbalance
  • Blood disorders
  • Confusion
  • Paraesthesia
  • Drowsiness
  • Respiratory disorders
  • Hearing loss
  • Vestibular dysfunction

Interactions

  • Other nephrotoxic drugs (e.g., vancomycin, furosemide)
  • Neuromuscular blocking agents
  • Other ototoxic agents

Precautions

  • Caution in renal impairment due to increased risk of nephrotoxicity and ototoxicity
  • Monitor renal function and auditory function before and during treatment
  • Use with caution in patients with existing hearing loss

Pregnancy

There is a risk of auditory or vestibular nerve damage in the infant when aminoglycosides, including streptomycin, are used during the second and third trimesters of pregnancy.

Breast-feeding

Streptomycin is excreted in breast milk; caution is advised when administering to nursing mothers.

Storage

Store below 25°C, protect from light, and keep out of reach of children.

Formulations

  • Streptomycin sulfate injection (various concentrations)
  • Streptomycin for inhalation (nebulized form)
  • Streptomycin oral solution
BNF 85 (British National Formulary) p.589 BNF for Children 2019-2020 p.345 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: Erythromycin

BNF-referenced

Erythromycin is a macrolide antibiotic effective against a range of bacterial infections. It works primarily by inhibiting protein synthesis in susceptible bacteria, making it a valuable choice for patients with penicillin hypersensitivity. Erythromycin is commonly used in treating respiratory tract infections, skin infections, and various other bacterial infections, including those caused by organisms like Propionibacterium acnes.

Indications

  • Bacterial infections
  • Acute otitis media
  • Community-acquired pneumonia
  • Skin and soft tissue infections
  • Campylobacter enteritis
  • Pertussis
  • Syphilis (early stage)
  • Chlamydia infections
  • Impetigo
  • Secondary bacterial infection of eczema

Dosage

Children: Child 1–23 months: 125 mg 4 times a day. Child 2–7 years: 250 mg 4 times a

Adults: 500 mg 4 times a day for 5 days, or alternatively 250–500 mg 4 times a day for 5–7 days.

Mechanism of action

Erythromycin exerts its antibacterial effect by binding to the 23S ribosomal RNA in the 50S subunit of bacterial ribosomes. This binding inhibits the transpeptidation and translocation steps of protein synthesis, effectively halting bacterial growth. The drug has a strong affinity for bacterial ribosomes, which contributes to its broad-spectrum activity against various pathogens.

Pharmacodynamics

Erythromycin acts as a bacteriostatic agent, preventing bacterial growth by inhibiting protein synthesis. It is effective against many strains of bacteria, although susceptibility testing is recommended due to increasing resistance. Notably, erythromycin does not impact nucleic acid synthesis and may lead to complications such as pseudomembranous colitis or hepatotoxicity in some patients.

Pharmacokinetics

Erythromycin is well-absorbed from the gastrointestinal tract, with bioavailability affected by food. It is widely distributed in body tissues, with higher concentrations in the lungs and liver. The drug undergoes hepatic metabolism and is primarily excreted in bile, with a small amount eliminated through urine. Erythromycin's half-life varies but generally ranges from 1.5 to 2 hours.

Contra-indications

  • Hypersensitivity to erythromycin or any component of the formulation
  • History of cholestatic jaundice or hepatic dysfunction associated with prior use of erythromycin

Adverse effects

  • Gastrointestinal disturbances (nausea, vomiting, diarrhea)
  • Cholestatic jaundice
  • Hepatotoxicity
  • Skin rashes
  • QT interval prolongation
  • Tinnitus
  • Hearing loss (reversible)
  • Pseudomembranous colitis

Interactions

  • Erythromycin may significantly increase the exposure to certain drugs such as antipsychotics, simvastatin, and triptans due to its effect on cytochrome P450 enzymes
  • Caution with concurrent use of drugs that prolong the QT interval
  • Moderate interaction with aminophylline (decreases exposure)

Precautions

  • Use with caution in patients with hepatic impairment or pre-existing liver disease
  • Monitor for signs of pseudomembranous colitis in patients with diarrhea following antibiotic use
  • Assess for potential drug interactions due to the impact on CYP450 metabolism

Pregnancy

Erythromycin crosses the placenta. It is generally considered safe for use during pregnancy, particularly for treating infections when no alternatives are available, but should be used with caution.

Breast-feeding

Erythromycin is excreted in breast milk. While generally considered safe, the infant should be monitored for potential side effects. Consult healthcare providers for specific recommendations.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children. Check specific product information for any temperature requirements.

Formulations

  • Oral suspension (125 mg/5 ml)
  • Tablets (250 mg and 500 mg)
  • Injectable solution (various strengths for intravenous administration)
BNF 85 (British National Formulary) p.614 BNF for Children 2019-2020 p.363 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: colistin

BNF-referenced

Colistin is a polymyxin antibiotic primarily used to treat infections caused by multidrug-resistant gram-negative bacteria. It acts as a surface-active agent that disrupts bacterial cell membranes, leading to cell death. Due to the emergence of antibiotic-resistant pathogens, colistin has regained importance in clinical settings, particularly for treating severe infections in patients with limited treatment options.

Indications

  • Treatment of multidrug-resistant gram-negative bacterial infections
  • Pneumonia caused by Pseudomonas aeruginosa
  • Complicated urinary tract infections
  • Infections in cystic fibrosis patients

Dosage

Children: Refer to the BNF for Children for appropriate paediatric dosing information.

Adults: Refer to the BNF for specific dosing guidelines, as doses may vary based on infection severity and renal function.

Mechanism of action

Colistin interacts with the bacterial cytoplasmic membrane, disrupting its integrity and altering permeability. It binds to the membrane through its cationic properties, leading to leakage of essential intracellular components, which results in bactericidal effects.

Pharmacodynamics

Colistin functions as a cationic polypeptide that disrupts bacterial cell membranes via a detergent-like mechanism. It is effective against certain multidrug-resistant organisms, including Pseudomonas aeruginosa and Acinetobacter baumannii. Its use has increased due to the rise of antibiotic-resistant infections, particularly in patients with cystic fibrosis and other serious infections.

Pharmacokinetics

Colistin is administered parenterally and has variable pharmacokinetics depending on the route of administration. It is not well-absorbed orally and is primarily eliminated by the kidneys. The pharmacokinetic profile may vary based on renal function and dosage regimen, necessitating careful monitoring in patients with renal impairment.

Adverse effects

  • Nephrotoxicity
  • Neurotoxicity
  • Allergic reactions
  • Rash
  • Fever

Interactions

  • Increased risk of nephrotoxicity with other nephrotoxic agents
  • Potential interactions with neuromuscular blockers

Precautions

  • Monitor renal function during treatment
  • Use with caution in patients with renal impairment
  • Consider monitoring neuromuscular function in patients receiving concomitant neuromuscular blockers

Pregnancy

Colistin should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

It is not known whether colistin is excreted in human milk. Caution should be exercised when administering to a nursing mother.

Storage

Store in a cool, dry place, away from light. Keep out of reach of children.

Formulations

  • Colistin sulfate for injection
  • Colistin methanesulfonate for injection

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: thiocyanate

BNF-referenced

Thiocyanate is an anion derived from thiocyanic acid, commonly found in various biological systems. It plays a role in sulfur metabolism and is involved in various biochemical pathways. Thiocyanate can be produced in the body through the metabolism of cyanide and is excreted primarily via the kidneys. Its presence in the body may reflect exposure to cyanogenic compounds or certain dietary sources, such as cruciferous vegetables.

Mechanism of action

Thiocyanate acts primarily by competing with iodide for uptake in the thyroid gland, thereby potentially inhibiting thyroid hormone synthesis. This can lead to a reduction in the production of thyroid hormones, affecting metabolic processes that are regulated by these hormones. Additionally, thiocyanate is involved in various metabolic pathways related to sulfur compounds, influencing overall redox status and metabolic homeostasis.

Pharmacodynamics

Thiocyanate has a notable effect on thyroid function due to its ability to inhibit iodide transport. This inhibition can result in decreased levels of thyroid hormones, which are crucial for regulating metabolism, growth, and development. The compound may also influence various metabolic pathways involving sulfur, interacting with enzymes and substrates related to sulfur metabolism.

Pharmacokinetics

Thiocyanate is absorbed through the gastrointestinal tract, and its distribution is influenced by factors such as protein binding and tissue uptake. The compound is primarily excreted through the kidneys, with renal clearance being a significant route of elimination. The half-life of thiocyanate can vary, but it is generally considered to be several days in the body, depending on individual metabolic rates and kidney function.

Pregnancy

Thiocyanate should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Thiocyanate is excreted in breast milk. Caution should be exercised when administering to nursing mothers.

Storage

Store in a tightly closed container at room temperature, away from heat and moisture.

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: Erythromycin

PubChem CID 12560

Molecular formula: C37H67NO13

Mechanism of action

In order to replicate, bacteria require a specific process of protein synthesis, enabled by ribosomal proteins. Erythromycin acts by inhibition of protein synthesis by binding to the 23S ribosomal RNA molecule in the 50S subunit of ribosomes in susceptible bacterial organisms. It stops bacterial protein synthesis by inhibiting the transpeptidation/translocation step of protein synthesis and by inhibiting the assembly of the 50S ribosomal subunit. This results in the control of various bacterial infections. The strong affinity of macrolides, including erythromycin, for bacterial ribosomes, supports their broad‐spectrum antibacterial activities. Macrolide antibiotics are bacteriostatic agents that inhibit protein synthesis by binding reversibly to 50S ribosomal subunits of sensitive microorganisms, at or very near the site that binds chloramphenicol. Erythromycin does not inhibit peptide bond formation per se, but rather inhibits the translocation step wherein a newly synthesized peptidyl tRNA molecule moves from the acceptor site on the ribosome to the peptidyl donor site. Gram-positive bacteria accumulate about 100 times more erythromycin than do gram-negative bacteria. Cells are considerably more permeable to the un-ionized form of the drug, which probably explains the increased antimicrobial activity at alkaline pH. ... /Erythromycin/ inhibits the growth of susceptible organisms (principally Propionibacterium acnes) on the surface of the skin and reduces the concn of free fatty acids in sebum ... The reduction in free fatty acids in sebum may be an indirect result of the inhibition of lipase-producing organisms which convert triglycerides into free fatty acids or may be a direct result of interference with lipase production in these organisms. /In acne treatment regimens/ Although stromal-derived factor-1 (SDF-1) via its cognate receptor CXCR4 is assumed to play a critical role in migration of endothelial cells during new vessel formation after tissue injury, CXCR4 expression on endothelial cells is strictly regulated. Erythromycin (EM), a 14-membered ring macrolide, has an anti-inflammatory effect that may account for its clinical benefit in the treatment of chronic inflammatory diseases. However, the effects of EM on endothelial cells and especially their expression of CXCR4 have not been fully evaluated. In this study, we demonstrated that EM markedly induced CXCR4 surface expression on microvascular endothelial cells in vitro and lung capillary endothelial cells in vivo. This ability to induce CXCR4 surface expression on endothelial cells was restricted to 14-membered ring macrolides and was not observed in other antibiotics including a 16-membered ring macrolide, josamycin. Furthermore, this EM-induced expression of CXCR4 on endothelial cells was functionally significant as demonstrated by chemotaxis assays in vitro. These findings suggest that EM-induced CXCR4 surface expression on endothelial cells may promote migration of CXCR4-expressing endothelial cells into sites of tissue injury, which may be associated with the known anti-inflammatory activity of this macrolide.

Pharmacodynamics

Macrolides, such as erythromycin, stop bacterial growth by inhibiting protein synthesis and translation, treating bacterial infections. Erythromycin does not exert effects on nucleic acid synthesis. This drug has been shown to be active against most strains of the following microorganisms, effectively treating both in vitro and clinical infections. Despite this, it is important to perform bacterial susceptibility testing before administering this antibiotic, as resistance is a common issue that may affect treatment. **A note on antimicrobial resistance, pseudomembranous colitis, and hepatotoxicity** Many strains of Haemophilus influenzae are resistant to erythromycin alone but are found to be susceptible to erythromycin and sulfonamides used in combination. It is important to note that Staphylococci that are resistant to erythromycin may emerge during erythromycin and/or sulfonamide therapy. Pseudomembranous colitis has been reported with most antibacterial agents, including erythromycin, and may range in severity from mild to life-threatening. Therefore, the physician should consider this diagnosis in patients with diarrhea after the administration of antibacterial agents. Erythromycin can cause hepatic dysfunction, cholestatic jaundice, and abnormal liver transaminases, particularly when erythromycin estolate is administered.

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

Molecular reference: Oxytetracycline

PubChem CID 54675779

Molecular formula: C22H24N2O9

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

Molecular reference: Streptomycin

PubChem CID 19649

Molecular formula: C21H39N7O12

Mechanism of action

There are 3 key phases of aminoglycoside entry into cells. The first “ionic binding phase” occurs when polycationic aminoglycosides bind electrostatically to negatively charged components of bacterial cell membranes including with lipopolysaccharides and phospholipids within the outer membrane of Gram-negative bacteria and to teichoic acids and phospholipids within the cell membrane of Gram-positive bacteria. This binding results in displacement of divalent cations and increased membrane permeability, allowing for aminoglycoside entry. The second “energy-dependent phase I” of aminoglycoside entry into the cytoplasm relies on the proton-motive force and allows a limited amount of aminoglycoside access to its primary intracellular target - the bacterial 30S ribosome. This ultimately results in the mistranslation of proteins and disruption of the cytoplasmic membrane. Finally, in the “energy-dependent phase II” stage, concentration-dependent bacterial killing is observed. Aminoglycoside rapidly accumulates in the cell due to the damaged cytoplasmic membrane, and protein mistranslation and synthesis inhibition is amplified. Hence, aminoglycosides have both immediate bactericidal effects through membrane disruption and delayed bactericidal effects through impaired protein synthesis; observed experimental data and mathematical modeling support this two-mechanism model. Inhibition of protein synthesis is a key component of aminoglycoside efficacy. Structural and cell biological studies suggest that aminoglycosides bind to the 16S rRNA in helix 44 (h44), near the A site of the 30S ribosomal subunit, altering interactions between h44 and h45. This binding also displaces two important residues, A1492 and A1493, from h44, mimicking normal conformational changes that occur with successful codon-anticodon pairing in the A site. Overall, aminoglycoside binding has several negative effects including inhibition of translation, initiation, elongation, and ribosome recycling. Recent evidence suggests that the latter effect is due to a cryptic second binding site situated in h69 of the 23S rRNA of the 50S ribosomal subunit. Also, by stabilizing a conformation that mimics correct codon-anticodon pairing, aminoglycosides promote error-prone translation. Mistranslated proteins can incorporate into the cell membrane, inducing the damage discussed above. The primary intracellular site of action of the aminoglycosides is the 30 S ribosomal subunit, which consists of 21 proteins and a single 16 S molecule of RNA. at least three of these proteins and perhaps the 16 S ribosomal RNA as well contribute to the streptomycin binding site, and alterations of these molecules markedly affect the binding and subsequent action of streptomycin. For example, a single amino acid substitution of asparagine for lysine at position 42 of one ribosomal protein (S12) prevents binding of the drug; the resultant mutant is totally resistant to streptomycin. Another mutant, in which glutamine is the amino acid at this position, is dependent on streptomycin. During protein synthesis, the ribosome selects aminoacyl-transfer RNAs with anticodons matching the messenger RNA codon present in the A site of the small ribosomal subunit. The aminoglycoside antibiotic streptomycin disrupts decoding by binding close to the site of codon recognition. Here we use X-ray crystallography to define the impact of streptomycin on the decoding site of the Thermus thermophilus 30S ribosomal subunit in complexes with cognate or near-cognate anticodon stem-loop analogues and messenger RNA. Our crystal structures display a significant local distortion of 16S ribosomal RNA induced by streptomycin, including the crucial bases A1492 and A1493 that participate directly in codon recognition. Consistent with kinetic data, we observe that streptomycin stabilizes the near-cognate anticodon stem-loop analogue complex, while destabilizing the cognate anticodon stem-loop analogue complex. These data reveal ho

Pharmacodynamics

Although streptomycin originally had broad gram-negative and gram-positive coverage, its spectrum of activity has been significantly narrowed due to antibiotic resistance. Streptomycins current spectrum of activity includes susceptible strains of Yersinia pestis, Francisella tularensis, Brucella, Calymmatobacterium granulomatis, H. ducreyi, H. influenza, K. pneumoniae pneumonia, E.coli, Proteus, A. aerogenes, K. pneumoniae, Enterococcus faecalis, Streptococcus viridans, Enterococcus faecalis, and Gram-negative bacillary bacteremia. Streptomycin is not reliably active against pseudomonas aeruginosa. Similar to other aminoglycosides, streptomycin is considered to have a narrow therapeutic index. Characteristic toxicities of streptomycin include nephrotoxicity and ototoxicity. Patients should be carefully monitored for early signs of hearing loss and vestibular dysfunction in order to prevent permanent damage to sensorineural cells. Neuromuscular blockade has also been rarely reported.

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

Molecular reference: colistin

PubChem CID 5311054

Molecular formula: C52H98N16O13

Mechanism of action

Colistin is a surface active agent which penetrates into and disrupts the bacterial cell membrane. Colistin is polycationic and has both hydrophobic and lipophilic moieties. It interacts with the bacterial cytoplasmic membrane, changing its permeability. This effect is bactericidal. There is also evidence that polymyxins enter the cell and precipitate cytoplasmic components, primarily ribosomes. POLYMYXIN B IS SURFACE-ACTIVE AGENT... CONTAINING LIPOPHILIC & LIPOPHOBIC GROUPS SEPARATED WITHIN MOLECULE. /POLYMYXIN B/ PERMEABILITY OF THE BACTERIAL MEMBRANE CHANGES IMMEDIATELY ON CONTACT WITH DRUG. SENSITIVITY TO POLYMYXIN B APPARENTLY IS RELATED TO THE PHOSPHOLIPID CONTENT OF THE CELL WALL-MEMBRANE COMPLEX. /POLYMYXIN B/ Colistin acts like a cationic detergent and binds to and damages the bacterial cytoplasmic membrane of susceptible bacteria. Damage to the bacterial cytoplasmic membrane alters the osmotic barrier of the membrane and causes leakage of essential intracellular metabolites and nucleosides.

Pharmacodynamics

Colistin is a polymyxin antibiotic agent. Polymyxins are cationic polypeptides that disrupt the bacterial cell membrane through a detergentlike mechanism. With the development of less toxic agents, such as extended-spectrum penicillins and cephalosporins, parenteral polymyxin use was largely abandoned, except for the treatment of multidrug-resistant pulmonary infections in patients with cystic fibrosis. More recently, however, the emergence of multidrug-resistant gram-negative bacteria, such as <i>Pseudomonas aeruginosa</i> and <i>Acinetobacter baumannii</i>, and the lack of new antimicrobial agents have led to the revived use of the polymyxins.

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

This drug in other countries

The same active ingredient registered across other registries we cover - including different brands.