Chlorool Capsule

An antibiotic first isolated from cultures of Streptomyces venequelae in 1947 but now produced synthetically. It has a relatively simple structure and was the first broad-spectrum antibiotic to be discovered. It acts by interfering with bacterial protein synthesis and is mainly bacteriostatic. (From Martindale, The Extra Pharmacopoeia, 29th ed, p106)

Chlorool Capsule 250 mg is a broad spectrum antibiotic that is effective against a variety of susceptible and serious bacterial infections but is not frequently used because of its high risk of bone marrow toxicity.

Used in treatment of cholera, as it destroys the vibrios and decreases the diarrhea. It is effective against tetracycline-resistant vibrios. It is also used in eye drops or ointment to treat bacterial conjunctivitis.

• Acne
• Bacterial Conjunctivitis
• Bacterial Conjunctivitis caused by susceptible bacteria
• Bacterial Infections
• Bacterial dacryocystitis
• Bacterial diarrhoea
• Conjunctivitis allergic
• Corneal Inflammation
• Eye swelling
• Keratitis bacterial
• Ocular Inflammation
• Trachoma
• Anterior eye segment inflammation
• Bacterial blepharitis
• Bacterial corneal ulcers
• Non-purulent ophthalmic infections caused by susceptible bacteria
• Superficial ocular infections
• Skin disinfection

Chlorool Capsule 250 mg is a broad-spectrum antibiotic that was derived from the bacterium Streptomyces venezuelae and is now produced synthetically. Chlorool Capsule 250 mg is effective against a wide variety of microorganisms, but due to serious side-effects (e.g., damage to the bone marrow, including aplastic anemia) in humans, it is usually reserved for the treatment of serious and life-threatening infections (e.g., typhoid fever). Chlorool Capsule 250 mg is bacteriostatic but may be bactericidal in high concentrations or when used against highly susceptible organisms. Chlorool Capsule 250 mg stops bacterial growth by binding to the bacterial ribosome (blocking peptidyl transferase) and inhibiting protein synthesis.

Chlorool Capsule 250 mg is lipid-soluble, allowing it to diffuse through the bacterial cell membrane. It then reversibly binds to the L16 protein of the 50S subunit of bacterial ribosomes, where transfer of amino acids to growing peptide chains is prevented (perhaps by suppression of peptidyl transferase activity), thus inhibiting peptide bond formation and subsequent protein synthesis.

Rapidly and completely absorbed from gastrointestinal tract following oral administration (bioavailability 80%). Well absorbed following intramuscular administration (bioavailability 70%). Intraocular and some systemic absorption also occurs after topical application to the eye.

Plasma protein binding is 50-60% in adults and 32% is premature neonates.

Half-life in adults with normal hepatic and renal function is 1.5 - 3.5 hours. In patients with impaired renal function half-life is 3 - 4 hours. In patients with severely impaired hepatic function half-life is 4.6 - 11.6 hours. Half-life in children 1 month to 16 years old is 3 - 6.5 hours, while half-life in infants 1 to 2 days old is 24 hours or longer and is highly variable, especially in low birth-weight infants.

Oral, mouse: LD₅₀ = 1500 mg/kg; Oral, rat: LD₅₀ = 2500 mg/kg. Toxic reactions including fatalities have occurred in the premature and newborn; the signs and symptoms associated with these reactions have been referred to as the gray syndrome. Symptoms include (in order of appearance) abdominal distension with or without emesis, progressive pallid cyanosis, vasomotor collapse frequently accompanied by irregular respiration, and death within a few hours of onset of these symptoms.

• Take on an empty stomach.