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Last updated:2024-05-08 14:48:35

Chloramphenicol Properties

Melting point 148-150 °C(lit.)
Boiling point 644.9±55.0 °C(Predicted)
alpha 19.5 º (c=6, EtOH)
Density 1.6682 (rough estimate)
refractive index 20 ° (C=5, EtOH)
Flash point 14 °C
storage temp. Keep in dark place,Inert atmosphere,2-8°C
solubility absolute ethanol: soluble5-20mg/mL (as a stock solution)
pka 11.03±0.46(Predicted)
form powder
color white
Water Solubility 2.5 g/L (25 º C)
Merck 14,2077
BRN 2225532
BCS Class 3
LogP 1.140
CAS DataBase Reference 56-75-7(CAS DataBase Reference)
FDA 21 CFR 530.41
NCI Dictionary of Cancer Terms CAF
NIST Chemistry Reference Chloramphenicol(56-75-7)
ATC code D06AX02,D10AF03,G01AA05,J01BA01,S01AA01,S02AA01,S03AA08
IARC 2A (Vol. Sup 7, 50) 1990
EPA Substance Registry System Chloramphenicol (56-75-7)

Pharmacokinetic data

Protein binding 60%
Excreted unchanged in urine 5-10%
Volume of distribution 0.5-1(L/kg)
Biological half-life 1.5-4 / Unchanged


Risk and Safety Statements

Symbol(GHS)  GHS hazard pictogramsGHS hazard pictograms
Signal word  Danger
Hazard statements  H318-H351-H361fd
Precautionary statements  P202-P280-P305+P351+P338-P308+P313-P405-P501
Hazard Codes  T,F
Risk Statements  45-11-39/23/24/25-23/24/25
Safety Statements  53-45-16-36/37
RIDADR  2811
WGK Germany  3
RTECS  AB6825000
HazardClass  3
HazardClass  IRRITANT
HS Code  29414000
Toxicity LD50 oral in rat: 2500mg/kg
NFPA 704
2 0

Chloramphenicol price More Price(66)

Manufacturer Product number Product description CAS number Packaging Price Updated Buy
Sigma-Aldrich 1107004 Chloramphenicol United States Pharmacopeia (USP) Reference Standard 56-75-7 200mg $436 2024-03-01 Buy
Sigma-Aldrich SRP5116 PCAF (431-end), GST tagged human recombinant, expressed in E. coli, ≥70% (SDS-PAGE), buffered aqueous glycerol solution 56-75-7 50μg $488 2023-06-20 Buy
Sigma-Aldrich 220551 Chloramphenicol - CAS 56-75-7 - Calbiochem Chloramphenicol, CAS 56-75-7, is a synthetic bacteriostatic antibiotic that inhibits the translation of RNA by blocking the peptidyltransferase reaction on ribosomes. 56-75-7 25g $75.3 2022-05-15 Buy
Sigma-Aldrich 220551 Chloramphenicol - CAS 56-75-7 - Calbiochem Chloramphenicol, CAS 56-75-7, is a synthetic bacteriostatic antibiotic that inhibits the translation of RNA by blocking the peptidyltransferase reaction on ribosomes. 56-75-7 100g $240 2022-05-15 Buy
Sigma-Aldrich 220551 Chloramphenicol - CAS 56-75-7 - Calbiochem Chloramphenicol, CAS 56-75-7, is a synthetic bacteriostatic antibiotic that inhibits the translation of RNA by blocking the peptidyltransferase reaction on ribosomes. 56-75-7 500g $814 2022-05-15 Buy
Product number Packaging Price Buy
1107004 200mg $436 Buy
SRP5116 50μg $488 Buy
220551 25g $75.3 Buy
220551 100g $240 Buy
220551 500g $814 Buy

Chloramphenicol Chemical Properties,Uses,Production


Chloramphenicol, also known as chlornitromycin, is a broad-spectrum, bacteriostatic antibiotic derived from Streptomyces venezuelae. It is first isolated from cultures of Streptomyces venequelae in 1947 but now produced synthetically. The synthetic product is racemic, also called synthomycin. Syntomycin is a mixture of chloramphenicol L-isomer and d-isomer. Because of dextroisomer antibacterial effect, the effect of synthomycin is only half of the natural products. It has a relatively simple structure and was the first broad-spectrum antibiotic to be discovered. It is effective against several gram-positive and gram-negative bacteria and commonly used in researching protein synthesis and to select for chloramphenicol-resistant transformed cells or the bacterial CAT gene.
Chloramphenicol is a semisynthetic, broad-spectrum antibiotic derived from Streptomyces venequelae with primarily bacteriostatic activity. Chloramphenicol diffuses through the bacterial cell wall and reversibly binds to the bacterial 50S ribosomal subunit. The binding interferes with peptidyl transferase activity, thereby prevents transfer of amino acids to the growing peptide chains and blocks peptide bond formation. As a result bacterial protein synthesis is blocked and impede bacterial cell proliferation.

Chemical Properties

It is white or yellowish green needle like crystals. The melting point is 150.5-151.5℃ (149.7-150.7℃). Under the high vacuum it can be sublimated, slightly soluble in water (2.5mg/ml at 25℃), slightly soluble in propylene glycol (150.8mg/ml), soluble in methanol, ethanol, butanol, ethyl acetate, acetone, insoluble in ether, benzene, petroleum ether, vegetable oil. Taste is very bitter.


  1. Chloramphenicol is used for the treatment caused by typhoid bacillus, dysentery bacillus, Escherichia coli, bacillus, influenza and pneumococcal infections such as brucellosis.
  2. Chloramphenicol is used in the treatment of infections caused by bacteria. It works by killing bacteria or preventing their growth.
  3. Chloramphenicol is used to treat serious infections in different parts of the body. It is sometimes given with other antibiotics. However, chloramphenicol should not be used for colds, flu, other virus infections, sore throats or other minor infections, or to prevent infections.
  4. Chloramphenicol should only be used for serious infections in which other medicines do not work. This medicine may cause some serious side effects, including blood problems and eye problems. Symptoms of the blood problems include pale skin, sore throat and fever, unusual bleeding or bruising, and unusual tiredness or weakness.
You and your doctor should talk about the good this medicine will do as well as the risks of taking it .
Chloramphenicol is available only with your doctor's prescription.

Antimicrobial Spectrum

Chloramphenicol is bacteriostatic and a broad-spectrum antibiotic active against both gram-positive and gram-negative bacteria including rickettsia (cause of rocky-mountain spotted fever) and chlamydia. It is also found effective against Haemophilus influenzae causing meningitis.

  1. Gram-positive: Streptococcus spp., Staphylococcus spp., Enterococcus spp., Bacillus anthracis, Listeria monocytogenes.
  2. Gram-negative: Hemophilus influenzae, M. catarrhalis, N. meningitides, E. coli, P. mirabilis, Salmonella spp., Shigella spp., Stenotrophomonas maltophilia.

Mechanism of action

Inhibition of protein synthesis, Chloramphenicol irreversibly binds to a receptor site on the 50S subunit of the bacterial ribosome, inhibiting peptidyl transferase. This inhibition consequently results to the prevention of amino acid transfer to growing peptide chains, ultimately leading to inhibition of protein formation.


After oral administration, it is rapidly and completely absorbed, can be widely distributed in body tissues and body fluids. In the cerebrospinal fluid concentration distribution were higher than other antibiotics, oral bioavailability was 75%~90%. After oral half hour of in the blood can reach the effective concentration, It can reach the peak in 2 to 3 hours. Take oral 0.5g, 1g and 2g, blood drug concentration was 4mg/L, 8~10mg/L and 16~21mg/L in 2 hours, 1~2g, 4 times a day, can make the blood to maintain long-term effective concentration of 10mg/L~5. After intravenous injection, the average is similarity with oral blood drug concentration of the same dose. After intramuscular absorption is slow and irregular, blood concentration is only oral amounts of 50%, but the maintenance time is long. The plasma protein binding rate is 50%~60%., the half-life of 2 to 3 hours, the half-life of newborns was significantly higher than that of adults, under the age of 2 is about 24 hours, 2 to 4 years is about 12 hours. This product is absorbed and widely distributed in the body each Reduce the concentrations of blood concentration in the blood to body fluids and tissues of liver and kidney was the highest, followed by the lung, spleen, heart, intestine and brain. Bile content is low, about 20%~50%, but also can enter the pleural effusion and ascites, milk, fetal circulation and ocular tissue. Through the blood brain barrier to reach the cerebrospinal fluid (CSF), in normal cerebrospinal fluid (CSF) in concentrations is up to 20%~50%, inflammation is up to 50%~100%. It is mainly in the liver metabolism, binding with glucuronic acid to inactivation, about 75%~90% of the metabolites in 24 hours urine, of which 5%~15% for the prototype drug. 1 g orally, urine concentration is 70~150mg/L. serious liver disease patients, the half-life may be extended due to hepatic metabolism and poisoning caused by accumulation.


This product is fat soluble, synthetic peptide can inhibit the formation and prevent protein. Is a bacteriostatic agent, high concentration or effect highly sensitive to the bacteria to this product showed bactericidal action. This product is applicable to the general application of typhoid and paratyphoid salmonella, and other Bacteroides fragilis.
1. Chloramphenicol is the preferred treatment of typhoid and paratyphoid fever, and can be used for typhoid Salmonella infections.
2. Used for pneumococcal in patients allergic to penicillin, ampicillin B Hib meningitis or tolerance, meningococcal meningitis, sensitive to the change of gram negative bacilli meningitis.
3. Used for aerobic and anaerobic bacteria mixed infection of otogenic brain abscess.
4. Used for serious anaerobic infections, such as Bacteroides fragilis infection.
5. Used as aminoglycoside drugs in the treatment of infection caused by sensitive bacteria and other microorganisms, such as influenza bacillus, Salmonella and other gram negative bacilli to sepsis, pulmonary infection.
6. Used for the local treatment of flu from Escherichia coli, bacillus, Klebsiella pneumoniae, Staphylococcus aureus, Streptococcus and eye, ear superficial infection.
7. It is effective for Rickettsia, mycoplasma, and infection.
8. Coli and Serratia of Pseudomonas aeruginosa is infections.
9. Chloramphenicol eye drops for the treatment of infections caused by sensitive bacteria caused by the eye, such as trachoma, conjunctivitis, keratitis, blepharitis etc..
10. This medicine local ear drops can be used for treating sensitive bacteria infections caused by otitis externa, acute and chronic otitis media, the drug ear plugs can also be for inflammation of the ear canal and radical mastoidectomy postoperative oozing pus.


Drug resistance of gram negative bacilli on chloramphenicol acetyltransferase, mostly due to drug inactivation, the enzyme is mediated by the R factor. Drug resistance of gram positive bacteria, may also be due to similar mechanisms, but not fully clear. Some strains of Pseudomonas aeruginosa and Proteus, Klebsiella, are another way to generate drug resistance, which prompted the permeability change, and chloramphenicol cannot enter the cell.
Bacterial resistance to chloramphenicol resistant strains both in vitro and in vivo, increased gradually in recent years. Escherichia coli, Salmonella and other gram negative bacilli can be due to drug resistance factor factor (R) transfer and acquire resistance. It has been proven that with R factor of Escherichia coli can produce acetyl transferase, chloramphenicol acetylation of failure; chloramphenicol resistant Staphylococcus aureus can also produce some inducible enzyme, under the participation of acetyl CoA, the acetylation of chloramphenicol.

Drug interactions

Chloramphenicol inhibits hepatic microsomal enzyme of phenytoin and tolbutamide (Jia Tangning) and chlorpropamide and dicoumarol (and possibly other drug metabolism, and the prolonged in vivo half-life, increased concentrations of serum. Poisoning aggravate that death is also reported. On the other side, phenobarbital, phenytoin, rifampin (are, 1985) can decrease the serum concentration of chloramphenicol, which was estimated to be due to the inductive effect of drugs on the liver enzymes. Therefore, at the same time, the application effect of chloramphenicol pharmacokinetics of drugs, should be paid attention to the monitoring of serum concentration of chloramphenicol.
Chloramphenicol can delay the iron, folic acid and vitamin B12 on anemia treatment response. It can interfere with the host to tetanus toxoid anamnestic response. Therefore, at the same time, the application situation chloramphenicol and active immune agents should be avoided.
Antagonistic effects of chloramphenicol on penicillin bactericidal effect, which is verified in vitro and animal experiments, but its clinical significance is not clear. This kind of combination, only in the proof of such treatment is benefit, began to be used.

Adverse reactions and precautions

1. Inhibition of bone marrow hematopoietic function: for the most serious toxicity of chloramphenicol, such as red blood cells, granulocyte and platelet reduce. There are two types: one is the reversible inhibition, manifested as neutropenia and thrombocytopenia, and anemia, related to dose and duration can be gradually recovered after drug withdrawal; Second is irreversible aplastic anemia, with dosage and duration without direct relationship, low incidence, once often occur difficult to reverse, high mortality rate and a few survivors can development for granulocytic leukemia, women, children, and liver and kidney function not entire occurrence rate is high. This is the main reason to limit the clinical application.
2. In the liver, metabolism rate of this product is very high, on the function of the liver, it has impaired the appropriate quantity (adult day not more than 1 g) or not as much as possible.
3. Chloramphenicol is only 5%~10% prototype drug discharge from the kidney, it is not appropriate for the treatment of urinary tract infection.
4. Premature infants and neonatal as much as possible.
5. I see the spirit of neurological symptoms, should be promptly discontinued.
6. During late pregnancy and lactation are not suitable for this application, because this product in vivo is conjugated with glucuronic acid and detoxification, conjugates excreted by the kidneys. And this product can be through the placenta to the fetus, fetal and neonatal, due to not perfect of enzyme system in the liver, glucuronic acid combined with the ability is poor and excretory function of the kidney is weak. Therefore, it is very easy to cause drug accumulation, the newborn gray baby syndromes. Gray cyanosis, dyspnea, vomiting, abdominal distension and circulatory failure with unique performance, high fatality rate. In addition, this product can damage the hematopoietic system, can make the pregnant women aplastic anemia, neonatal thrombocytopenia and other consequences.

Methods of production

Methods for producing countries in the world to chloramphenicol had a lot of research, summed up: (1) p-nitroacetophenone method; (2) styrene method; (3) Cinnamyl alcohol method; (4) The nitro cinnamic alcohol method; (5) P-nitrobenzaldehyde method. China use p-nitroacetophenone method, the method is by ethylbenzene via nitration, oxidation, bromide, salt, hydrolysis, acetylation, addition, reduction, decomposition, split second chloride acetylation and chloramphenicol.


Chloramphenicol was originally produced by fermentation of Streptomyces venezuelae, but its comparatively simple chemical structure soon resulted in several efficient total chemical syntheses. With two asymmetric centers, it is one of four diastereomers, only one of which (1R,2R) is significantly active. Because total synthesis produces a mixture of all four, the unwanted isomers must be removed before use. Chloramphenicol is a neutral substance that is only moderately soluble in water, because both nitrogen atoms are nonbasic under physiologic conditions (one is an amide and the other a nitro moiety). It was the first broad-spectrum oral antibiotic used in the United States and was once very popular. Severe potential blood dyscrasia has greatly decreased its use in North America. Although its cheapness and efficiency makes it still very popular in much of the rest of the world where it can often be purchased over-the-counter without a prescription

Chemical Properties

White to grey-white crystalline powder

Chemical Properties

Chloramphenicol is a white to grayish-white or yellowish-white crystalline solid.


Leukomycin,Bayer,W. Germany


antibacterial, antirickettsial, inhibits protein synthesis


Broad spectrum antibiotic obtained from cultures of the soil bacterium Streptomyces venezuelae. It has a broad spectrum of activity against Gram-positive and gram-negative bacteria. Antibacterial; antirickettsial


Chloramphenicol is unusual nitroaromatic metabolite produced by Streptomyces venezuelae, first published in 1947. Chloramphenicol is a broad spectrum antibiotic with good activity against Gram negative and anaerobic bacteria. Although restricted to ocular use, antibiotic resistance to other classes has refocused attention on this class. Chloramphenicol acts by binding to the 23S sub-unit of the 50S ribosome, inhibiting protein synthesis. Chloramphenicol has been extensively studied with over 35,000 literature citations.


ChEBI: Chloramphenicol is an organochlorine compound that is dichloro-substituted acetamide containing a nitrobenzene ring, an amide bond and two alcohol functions. It has a role as an antimicrobial agent, an antibacterial drug, a protein synthesis inhibitor, an Escherichia coli metabolite, a Mycoplasma genitalium metabolite and a geroprotector. It is an organochlorine compound, a diol, a C-nitro compound and a carboxamide.


Resistance to chloramphenicol is usually explained by the presence of a plasmid that determines the production of chloramphenicol acetyltransferase. This enzyme acetylates the drug, giving it unable to bind with 50 S subunits of bacterial ribosomes.
Chloramphenicol is a potentially toxic drug and has a few indications for use. It is the drug of choice for treating typhoid fever, and it is used for treating brain abscesses. Until recently, it was the drug of choice for therapy of bacterial meningitis in children (in combination with ampicillin). However, third-generation cephalosporins are currently preferred for such purposes. Chloramphenicol is an effective alternative for a number of infections in situations, where drugs of choice cannot be used for one reason or another. However, it should never be used for infections that can readily be treated with other antimicrobial drugs. Synonyms of this drug are levomycetin, amindan, aquamycetin, chloromycetin, ophthoclor, opulets, leukomycin, and many others.

Manufacturing Process

Chloramphenicol may be prepared by fermentation or by chemical synthesis. The fermentation route to chloramphenicol is described in US Patents 2,483,871 and 2,483,892. To quote from US Patent 2,483,892: The cultivation of Streptomyces venezuelae may be carried out in a number of different ways. For example, the microorganism may be cultivated under aerobic conditions on the surface of the medium, or it may be cultivated beneath the surface of the medium, i.e., in the submerged condition, if oxygen is simultaneously supplied.
Briefly stated, the production of chloramphenicol by the surface culture method involves inoculating a shallow layer, usually less than about 2 cm, of a sterile, aqueous nutrient medium with Streptomyces venezuelae and incubating the mixture under aerobic conditions at a temperature between about 20° and 40°C, preferably at room temperature (about 25°C), for a period of about 10 to 15 days. The mycelium is then removed from the liquid and the culture liquid is then treated by methods described for isolating therefrom the desired chloramphenicol. The synthetic route to chloramphenicol is described in US Patent 2,483,884 as follows: 1.1 g of sodium is dissolved in 20 cc of methanol and the resulting solution added to a solution of 5 g of benzaldehyde and 4.5 g of betanitroethanol in 20 cc of methanol. After standing at room temperature for a short time the gel which forms on the mixing of the reactants changes to a white insoluble powder. The precipitate is collected, washed with methanol and ether and then dried. The product thus produced is the sodium salt of 1- phenyl-2-nitropropane-1,3-diol.
Eighteen grams of the sodium salt of 1-phenyl-2-nitropropane-1,3-diolis dissolved in 200 cc of glacial acetic acid. 0.75 g of palladium oxide hydrogenation catalyst is added and the mixture shaken at room temperature under three atmospheres pressure of hydrogen overnight. The reaction vessel is opened, 2.5 g of 10% palladium on carbon hydrogenation catalyst added and the mixture shaken under three atmospheres pressure of hydrogen for 3 hours. The catalyst is removed from the reaction mixture by filtration and the filtrate concentrated under reduced pressure. Fifty cubic centimeters of npropanol is added to the residue and the insoluble inorganic salt removed by filtration.
The filtrate is treated with excess hydrochloric acid and evaporated to obtain a pale yellow oil. Five grams of the oil thus obtained is treated with 15 cc of saturated potassium carbonate solution and the mixture extracted with 50 cc of ether, then with 30 cc of ethyl acetate and finally with two 30 cc portions of ethanol. Evaporation of the solvent from the extract gives the following quantities of the desired 1-phenyl-2-aminopropane-1,3-diol: 0.5 g, 1.0 g and 3.1 g.
1.7 g of 1-phenyl-2-aminopropane-1,3-diol is treated with 1.6 g of methyl dichloroacetate and the mixture heated at 100°C for 1.25 hours. The residue is washed with two 20 cc portions of petroleum ether and the insoluble product collected. Recrystallization from ethyl acetate yields the desired (dl)- reg.-1-phenyl-2-dichloroacetamidopropane-1,3-diol in pure form; MP 154° to 156°C.Five hundred milligrams of (dl)-reg.-1-phenyl-2-dichloroacetamidopropane- 1,3-diolis added to a solution consisting of 1 cc of pyridine and 1 cc of acetic anhydride and the resulting reaction mixture heated at 100°C for 1/2 hour. The reaction mixture is evaporated to dryness under reduced pressure and the residue taken up in and crystallized from methanol. Recrystallization from methanol produces the pure diacetate of (dl)-reg.-1-phenyl-2-dichloroacetamidopropane-1,3-diol (MP 94°C). Two hundred milligrams of the diacetate of (dl)-reg.-1-phenyl-2- dichloroacetamidopropane1,3-diol is added to a mixture consisting of 0.25 cc of concentrated nitric acid and 0.25 cc of concentrated sulfuric acid at 0°C. The reaction mixture is stirred until solution is complete, poured onto 25 g of ice and the mixture extracted with ethyl acetate. The ethyl acetate extracts are evaporated under reduced pressure and the diacetate of (dl)-reg.-1- pnitrophenyl-2-dichloroacetamidopropane-1,3-diol so produced purified by recristallization from ethanol; MP 134°C.
Five hundred milligrams of the diacetate of (dl)-reg.-1-p-nitrophenyl-2- dichloroacetamidopropane-1,3-diol is dissolved in a mixture consisting of 25 cc of acetone and an equal volume of 0.2 N sodium hydroxide solution at 0°C and the mixture allowed to stand for one hour. The reaction mixture is neutralized with hydrochloric acid and evaporated under reduced pressure to dryness. The residue is extracted with several portions of hot ethylene dichloride, the extracts concentrated and then cooled to obtain the crystalline (dl)-reg.-1- p-nitrophenyl-2-dichloroacetamidopropane-1,3-diol; MP 171°C.

brand name

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Therapeutic Function


World Health Organization (WHO)

Chloramphenicol, an antibiotic isolated from Streptomyces venezuelae in 1947, first became available for general clinical use in 1948. By 1950 it was evident that its use could cause serious, sometimes fatal, blood dyscrasias. However, it remains one of the most effective antibiotics for treating invasive typhoid fever and salmonellosis, some rickettsioses and serious infections caused by Haemophilus influenzae or anaerobic organisms. This is considered to justify its retention in the WHO Model List of Essential Drugs. (Reference: (WHTAC1) The Use of Essential Drugs, 2nd Report of the WHO Expert Committee, 722, , 1985)

Antimicrobial activity

It is active against a very wide range of organisms. Minimum inhibitory concentrations (MICs) (mg/L) for other organisms are: Staphylococcus epidermidis, 1–8; Corynebacterium diphtheriae, 0.5–2; Bacillus anthracis, 1–4; Clostridium perfringens, 2–8; Mycobacterium tuberculosis, 8–32; Legionella pneumophila, 0.5–1; Bordetella pertussis, 0.25–4; Brucella abortus, 1–4; Campylobacter fetus, 2–4; Pasteurella spp., 0.25–4; Serratia marcescens, 2–8; Burkholderia pseudomallei, 4–8. Most Gramnegative bacilli are susceptible, but Pseudomonas aeruginosa is resistant. Leptospira spp., Treponema pallidum, chlamydiae, mycoplasmas and rickettsiae are all susceptible, but Nocardia spp. are resistant. It is widely active against anaerobes, including Actinomyces israelii (MIC 1–4 mg/L), Peptostreptococcus spp. (MIC 0.1–8 mg/L), and Fusobacterium spp. (MIC 0.5–2 mg/L), but Bacteroides fragilis is only moderately susceptible (MIC about 8 mg/L).
It is strictly bacteristatic against almost all bacterial species, but exerts a bactericidal effect at 2–4 times the MIC against some strains of Gram-positive cocci, Haemophilus influenzae and Neisseria spp. The minimum bactericidal concentrations (MBCs) for penicillin-resistant pneumococci are often significantly higher than those for penicillin- susceptible strains, although this cannot be detected by conventional disk susceptibility testing or MIC determination. Its bacteristatic effect may inhibit the action of penicillins and other β-lactam antibiotics against Klebsiella pneumoniae and other enterobacteria in vitro, but the clinical significance of this is doubtful. The presence of ampicillin does not affect the bactericidal effect of chloramphenicol on H. influenzae.

Acquired resistance

The prevalence of resistant strains in many Gram-positive and Gram-negative organisms reflects usage of the antibiotic. Over-the-counter sales are believed to have compounded the problem in some countries. For example, it has long been the drug of choice for the treatment of typhoid and paratyphoid fevers, but widespread use led to a high prevalence of resistant Salmonella enterica serotype Typhi. Outbreaks of infection caused by chloramphenicol-resistant S. Typhi have been seen since the early 1970s. Use of co-trimoxazole and fluoroquinolones in typhoid has resulted in a decline in chloramphenicol resistance in some endemic areas. Many hospital outbreaks caused by multiresistant strains of enterobacteria, notably Enterobacter, Klebsiella and Serratia spp., have been described.
Plasmid-borne resistance was first noted in shigellae in Japan and subsequently spread widely in Central America, where it was responsible for a huge outbreak. Strains of S. Typhi resistant to many antibiotics including chloramphenicol are particularly common in the Indian subcontinent. Resistance in shigellae is also relatively common in some parts of the world.
Resistant strains of H. influenzae (some also resistant to ampicillin), Staph. aureus and Streptococcus pyogenes are also encountered. Most N. meningitidis strains remain susceptible,but high-level resistance (MIC >64 mg/L) due to the production of chloramphenicol acetyltransferase has been described; the nucleotide sequence of the resistance gene was indistinguishable from that found on a transposon in Cl. perfringens. Resistant strains of Enterococcus faecalis are relatively common, and resistance to chloramphenicol is found in some multiresistant pneumococci.
Resistance in Staph. aureus is caused by an inducible acetyltransferase; additionally, the cfr (chloramphenicol– florfenicol resistance) gene encodes a 23S rRNA methyltransferase that also confers resistance to linezolid. In Escherichia coli, the capacity to acetylate chloramphenicol (at least three enzymes are involved) is carried by R factors. Replacement of the 3-OH group, which is the target of acetylation, accounts for the activity of fluorinated analogs against strains resistant to chloramphenicol and thiamphenicol. The resistance of B. fragilis and some strains of H. influenzae is also due to elaboration of a plasmid-encoded acetylating enzyme; in others it is due to reduced permeability resulting from loss of an outer membrane protein. Some resistant bacteria reduce the nitro group or hydrolyze the amide linkage. Resistance of Ps. aeruginosa is partly enzymic and partly due to impermeability.

General Description

Synthetic bacteriostatic antibiotic that inhibits the translation of RNA by blocking the peptidyltransferase reaction on ribosomes.


Has deleterious and dangerous side effects. Must conform to FDA labeling requirements. Use is closely restricted. Probable carcinogen.

Biochem/physiol Actions

Potency: ≥970 μg/mg

Contact allergens

This broad spectrum phenicol group antibiotic has been implicated in allergic contact dermatitis. Cross-sensitivity to thiamphenicol is possible, but not systematic.

Mechanism of action

Chloramphenicol is bacteriostatic by virtue of inhibition of protein biosynthesis in both bacterial and, to a lesser extent, host ribosomes. Chloramphenicol binds to the 50S subparticle in a region near where the macrolides and lincosamides bind.
Resistance is mediated by several R-factor enzymes that catalyze acetylation of the secondary and, to some extent, the primary hydroxyl groups in the aliphatic side chain. These products no longer bind to the ribosomes and so are inactivated. Escherichi a coli frequently is resistant because of chloramphenicol's lack of intercellular accumulation.


Oral absorption: 80–90%
Cmax 500 mg oral: 10–13 mg/L after 1–2 h
Plasma half-life: 1.5–3.5 h
Volume of distribution: 0.25–2 L/kg
Plasma protein binding: c. 25–60%
The plasma concentration achieved is proportional to the dose administered. Suspensions for oral administration to children contain chloramphenicol palmitate, a tasteless and bacteriologically inert compound, which is hydrolyzed in the gut to liberate chloramphenicol. Following a dose of 25 mg/kg, peak plasma levels around 6–12 mg/L are obtained, but there is much individual variation.
Pancreatic lipase is deficient in neonates and, because of poor hydrolysis, the palmitate should be avoided. In very young infants, deficient ability to form glucuronides, and low glomerular and tubular excretion greatly prolong the plasma half-life. For parenteral use, chloramphenicol sodium succinate, which is freely soluble and undergoes hydrolysis in the tissues with the liberation of chloramphenicol, can be injected intravenously or in small volumes intramuscularly. The plasma concentrations after administration by these routes are unpredictable, and approximate to only 30–70% of those obtained after the same dose by the oral route. Protein binding is reduced in cirrhotic patients and neonates, with correspondingly elevated concentrations of free drug.
Free diffusion occurs into serous effusions. Penetration occurs into all parts of the eye, the therapeutic levels in the aqueous humor being obtained even after local application of 0.5% ophthalmic solution. Concentrations obtained in cerebrospinal fluid (CSF) in the absence of meningitis are 30–50% of those of the blood and greater in brain. It crosses the placenta into the fetal circulation and appears in breast milk.
It is largely inactivated in the liver by conjugation with glucuronic acid or by reduction to inactive arylamines; clearance of the drug in patients with impaired liver function is depressed in relation to the plasma bilirubin level. It has been suggested that genetically determined variance of hepatic glucuronyl transferase might determine the disposition and toxicity of the drug.
It is excreted in the glomerular filtrate, and in the newborn elimination may be impaired by the concomitant administration of benzylpenicillin, which is handled early in life by the same route. Inactive derivatives are eliminated partly in the glomerular filtrate and partly by active tubular secretion. Over 24 h, 75–90% of the dose appears in the urine, 5–10% in biologically active forms and the rest as metabolites, chiefly as a glucuronide conjugate. Excretion diminishes linearly with renal function and at a creatinine clearance of <20 ml/min, maximum urinary concentrations are 10–20 mg/L rather than the 150–200 mg/L found in normal subjects. Because of metabolism, blood levels of active drug are only marginally elevated in renal failure, but microbiologically inactive metabolites accumulate. The plasma half-life of the products in the anuric patient is around 100 h, and little is removed by peritoneal or hemodialysis. Dosage modification is normally unnecessary in renal failure as the metabolites are less toxic than the parent compound. About 3% of the administered dose is excreted in the bile, but only 1% appears in the feces, and this mostly in inactive forms.
Induction of liver microsomal enzymes, for example by phenobarbital (phenobarbitone) or rifampicin (rifampin), diminishes blood levels of chloramphenicol; conversely, chloramphenicol, which inhibits hepatic microsomal oxidases, potentiates the activity of dicoumarol (dicumarol), phenytoin, tolbutamide and those barbiturates that are eliminated by metabolism. It also depresses the action of cyclophosphamide, which depends for its cytotoxicity on transformation into active metabolites. It is uncertain whether this interaction may lead to a clinically significant level of inhibition of the activity of cyclophosphamide. The half-life of chloramphenicol is considerably prolonged if paracetamol (acetaminophen) is given concurrently, and co-administration of these drugs should be avoided.

Clinical Use

Typhoid fever and other severe infections due to salmonellae
Rickettsial infections
Invasive infection caused by H. influenzae
Destructive lung lesions involving anaerobes
Eye infections (topical)
Reference is made to its use in cholera, plague, tularemia and bartonellosis, melioidosis, Whipple’s disease and relapsing fever. In enteric fever in adults, fluoroquinolones are associated with a lower clinical relapse rate. Treatment for other serious infections should be restricted to organisms that are resistant or much less susceptible to other antibiotics. A study in low resource countries found ampicillin plus gentamicin superior to injectable chloramphenicol for the treatment of very severe communityacquired pneumonia in children.
It has been used with varying success to treat infections caused by glycopeptide-resistant enterococci. Meningitis caused by penicillin-resistant pneumococci responds poorly, apparently due to failure to achieve bactericidal concentrations in CSF. It should never be given systemically for minor infections. Topical use in the treatment of eye infections is controversial given the unsubstantiated risk of bone marrow aplasia. A placebo-controlled study in children with infective conjunctivitis in the community found no clinical benefit in the use of chloramphenicol eye drops.
The daily dose should not normally exceed 2 g, and the duration of the course should be limited (e.g. 10 days). Although patients may show toxic manifestations after receiving very little drug, the danger is almost certainly increased by excessive or repeated dosage or by the treatment of patients with impaired hepatic or renal function, including those at the extremes of life. The wide pharmacokinetic variability of the antibiotic in neonates makes monitoring of serum concentrations advisable. Determination of full blood counts should be carried out twice weekly.

Side effects

Glossitis, associated with overgrowth of Candida albicans, is fairly common if the course of treatment exceeds 1 week. Stomatitis, nausea, vomiting and diarrhea may occur, but are uncommon. Hypersensitivity reactions are very uncommon. Jarisch–Herxheimer-like reactions have been described in patients treated for brucellosis, enteric fever and syphilis.
Bone marrow effects
Chloramphenicol exerts a dose-related but reversible depressant effect on the marrow of all those treated, resulting in vacuolization of erythroid and myeloid cells, reticulocytopenia and ferrokinetic changes indicative of decreased erythropoiesis. Evidence of bone-marrow depression is regularly seen if the plasma concentration exceeds 25 mg/L, and leukopenia and thrombocytopenia may be severe. There is no evidence that this common marrow depression is the precursor of potentially fatal aplasia, which differs in that it is fortunately rare, late in onset, usually irreversible and may follow the smallest dose. Aplasia can follow systemic, oral and even ophthalmic administration and may be potentiated by cimetidine. Liver disease, uremia and pre-existing bone marrow dysfunction may increase the risk. It is unusual for manifestations to appear during treatment, and the interval between cessation of treatment and onset of dyscrasia can be months. A few patients survive with protracted aplasia, and myeloblastic leukemia then often supervenes.
It is thought that the toxic agent is not chloramphenicol itself but an as yet unidentified metabolite. Chloramphenicol is partially metabolized to produce oxidized, reduced and conjugated products. The toxic metabolite may be a shortlived product of reduction of the nitro group, which damages DNA by helix destabilization and strand breakage.
Predisposition to aplasia may be explained by genetically determined differences in metabolism of the agent. Risk of fatal aplastic anemia has been estimated to increase 13-fold on average treatment with 4 g of chloramphenicol. Corresponding increases are 10-fold in patients treated with mepacrine (quinacrine) and 4-fold in patients treated with oxyphenbutazone.
Infants given large doses may develop exceedingly high plasma levels of the drug because of their immature conjugation and excretion mechanisms. A life-threatening disorder called the ‘gray baby’ syndrome, characterized by vomiting, refusal to suck and abdominal distention followed by circulatory collapse, may appear when the plasma concentration exceeds 20 mg/L. If concentrations reach 200 mg/L, the disorder can develop in older children or even adults.
Optic neuritis has been described in children with cystic fibrosis receiving prolonged treatment for pulmonary infection. Most improve when the drug is discontinued, but central visual acuity can be permanently impaired. There is some experimental evidence that ear drops containing 5% chloramphenicol sodium succinate can damage hearing. One study identified an increased risk of acute leukemia following childhood administration of chloramphenicol, particularly for durations exceeding 10 days.

Safety Profile

Confirmed human carcinogen producing leukemia, aplastic anemia, and other bone marrow changes. Experimental tumorigenic data. Poison by intravenous and subcutaneous routes. Moderately toxic by ingestion and intraperitoneal routes. Human systemic effects by an unknown route: changes in plasma or blood volume, unspecified liver effects, and hemorrhaging. Experimental teratogenic and reproductive effects. Human mutation data reported. An antibiotic. When heated to decomposition it emits very toxic fumes of NOx and Cl-. See also other chloramphenicol entries.


Chloramphenicol, D-threo-2,2-dichloro-N-[|?-hydroxy-|á-(hydroxymethyl)]-n-nitrophenylacetamide (32.6.7), was first isolated in 1947 from a culture fluid of the actinomycete Streptomyces venezuelae; however, it is only currently produced synthetically. When using a synthetic racemic mixture without having previously separated it into D- and L-threo forms, it is called sintomycin. Two ways of synthesizing chloramphenicol are suggested. The first begins with 4-nitroacetophenone, which is brominated with molecular bromine to make |?-bromo-4-nitroacetophenone (32.6.1). This is transformed to |?-amino- 4-nitroacetophenone (32.6.2) by successive production of a quaternary salt with urotropine and subsequent break up to an amine using hydrogen chloride. The resulting aminoketone is acylated with acetic anhydride to make |?-acetamido-4-nitroacetophenone (32.6.3), and the product undergoes acylmethylation with paraform aldehyde to give |á-acetamido- |?-hydroxy-4-nitropropiophenone (32.6.4). Reducing the carbonyl group in the resulting compound with aluminum isopropoxide in isopropyl alcohol gives D,L-threo-2-acetamido- 1-(4-nitrophenyl)-1,3-propandiol (32.6.5). The acetyl group is hydrolyzed in hydrochloric acid to form D,L-threo-2-amino-1(4-nitrophenyl)-1,3-propandiol. The resulting racemic mixture of amines is treated with camphor-D-sulfonic acid, and the resulting enantiomeric salts are separated. After alkaline hydrolysis of the selected salt, the product D, (?)-threo-2- amino-1-(4-nitrophenyl)-1,3-propandiol (32.6.6) is synthesized. Acylating the aminogroup of this compound with the methyl ester of dichloroacetic acid gives the desired chloramphenicol (32.6.7).


The other synthesis begins with cinnamic alcohol, which is reacted with hypobromous acid to make 2-bromo-1-phenyl-1,3-propandiol (32.6.8), the hydroxyl group of which is protected as a ketal by reacting it with acetone, giving 5-bromo-2,2-dimethyl-4-phenyl- 1,3-dioxane (32.6.9). Reacting the resulting bromide with ammonia gives an isomeric mixture of D,L-threo-5-amino-2,2-dimethyl-4-phenyl-1,3-dioxane, which upon treatment with D-tartaric acid, separation of the resulting salts, and subsequent alkaline hydrolysis of the selected salt gives D-(?)-5-amino-2,2-dimethyl-4-phenyl-1,3-dioxane (32.6.10). Acylating this with the methyl ester of dichloroacetic acid gives D-(?)-threo-5-dichloroacetamido-2,2-dimethyl-4-phenyl-1,3-dioxane (32.6.11). The phenyl ring is then nitrated, during which the 1,3-dioxane ring is cleaved off, giving dinitrate of D-(?)-threo-2- dichloroacetamido-1-(4-nitrophenyl)-1,3-propandiol (32.6.12). Reducing the nitro group in this compound with bivalent iron sulfate gives the desired chloramphenicol (32.6.7).


Potential Exposure

An antibiotic derived from streptomyces venezuelae. A potential danger to those involved in the manufacture, formulation, and application of this antibiotic and antifungal agent

Veterinary Drugs and Treatments

Chloramphenicol is used for a variety of infections in small animals and horses, particularly those caused by anaerobic bacteria. The FDA has prohibited the use of chloramphenicol in animals used for food production because of the human public health implications.

Drug interactions

Potentially hazardous interactions with other drugs
Anticoagulants: effect of coumarins enhanced.
Antidiabetics: effect of sulphonylureas enhanced.
Antiepileptics: metabolism accelerated by phenobarbital and primidone (reduced concentration of chloramphenicol); increased concentration of fosphenytoin and phenytoin (risk of toxicity).
Antipsychotics: avoid with clozapine (increased risk of agranulocytosis).
Ciclosporin: possibly increases ciclosporin concentration.
Clopidogrel: possibly reduces antiplatelet effect.
Tacrolimus: possibly increases tacrolimus concentration.

First aid

If this chemical gets into the eyes, remove anycontact lenses at once and irrigate immediately for at least15 min, occasionally lifting upper and lower lids. Seek med?ical attention immediately. If this chemical contacts theskin, remove contaminated clothing and wash immediatelywith soap and water. Seek medical attention immediately. Ifthis chemical has been inhaled, remove from exposure,begin rescue breathing (using universal precautions, includ?ing resuscitation mask) if breathing has stopped and CPR if598 Chloramphenicolheart action has stopped. Transfer promptly to a medicalfacility. When this chemical has been swallowed, get medical attention. Give large quantities of water and inducevomiting. Do not make an unconscious person vomit.


Chloramphenicol is reasonably anticipated to be a human carcinogen, based on limited evidence of carcinogenicity from studies in humans.

Environmental Fate

As an antibiotic, chloramphenicol enters the target cells by facilitated diffusion and binds reversibly to the 50S ribosomalsubunit. This prevents the interaction between peptidyl transferase and its amino acid substrate, which results in the inhibition of peptide bond formation. Indeed, it is an inhibitor of protein synthesis in the bacteria and to a lesser extent, in eukaryotic cells. Chloramphenicol can also inhibit mitochondrial protein synthesis in mammalian cells particularly erythropoietic cells, which are sensitive to the drug.

Metabolic pathway

Six metabolites of chloramphenicol are identified, among which the sulfate conjugate is characterized in goat urine.


When given orally, it is rapidly and completely absorbed but has a fairly short half-life. It is mainly excreted in the urine in the form of its metabolites, which are a C-3 glucuronide, and, to a lesser extent, its deamidation product and the product of dehalogenation and reduction. These metabolites are all inactive. The aromatic nitro group also is reduced metabolically, and this product can undergo amide hydrolysis. The reduction of the nitro group, however, does not take place efficiently in humans but, rather, primarily occurs in the gut by the action of the normal flora. Chloramphenicol potentiates the activity of some other drugs by inducing liver metabolism. Such agents include anticoagulant coumarins, sulfonamides, oral hypoglycemics, and phenytoin.


Color Code—Blue: Health Hazard/Poison: Storein a secure poison location. Prior to working withChloramphenicol you should be trained on its proper handling and storage. A regulated, marked area should beestablished where this chemical is handled, used, or storedin compliance with OSHA Standard 1910.1045. Store intightly closed containers in a cool, well-ventilated area.


UN3249 Medicine, solid, toxic, n.o.s., Hazard Class: 6.1; Labels: 6.1-Poisonous materials. UN2811 Toxic solids, organic, n.o.s., Hazard Class: 6.1; Labels: 6.1- Poisonous materials, Technical Name Required.

Purification Methods

Purify chloramphenicol by recrystallisation from H2O (solubility is 2.5mg/mL at 25o) or ethylene dichloride as needles or long plates, and by sublimation at high vacuum. It has A 1cm 298 at max 278nm, and it is slightly soluble in H2O (0.25%) and propylene glycol (1.50%) at 25o but is freely soluble in MeOH, EtOH, BuOH, EtOAc and Me2CO. [Relstock et al. J Am Chem Soc 71 2458 1949, Confroulis et al. J Am Chem Soc 71 2463 1949, Long & Troutman J Am Chem Soc 71 2469, 2473 1949, Ehrhart et al. Chem Ber 90 2088 1957, Beilstein 13 IV 2742.]

Toxicity evaluation

In the aquatic system, chloramphenicol is not expected to adsorb to suspended solids and sediments given by the Koc (Soil Organic Carbon–Water Partitioning Coefficient) value of 99.
Chloramphenicol solutions are susceptible to direct photolysis by sunlight or high temperatures and decompose to form hydrochloric and dichloric acid. Hydrolysis of chloramphenicol is not anticipated under environmental conditions because it lacks a functional group to hydrolyze. Chloramphenicol has been reported to degrade 86.2% with a biodegradation rate of 3.3 mg COD per gram per hour using adapted activated sludge as the inoculums. It can also be degraded by intestinal bacteria via amidolysis to 18 observed metabolites.


Compounds of the carboxyl group react with all bases, both inorganic and organic (i.e., amines), releasing substantial heat, water, and a salt that may be harmful. Incompatible with arsenic compounds (releases hydrogen cyanide gas), diazo compounds, dithiocarbamates, isocyanates, mercaptans, nitrides, sulfides (releasing heat, toxic, and possibly flammable gases), thiosulfates, and dithionites (releasing hydrogen sulfate and oxides of sulfur).

Waste Disposal

It is inappropriate and possibly dangerous to the environment to dispose of expired or waste pharmaceuticals by flushing them down the toilet or discarding them to the trash. Household quantities of expired or waste pharmaceuticals may be mixed with wet cat litter or coffee grounds, double-bagged in plastic, discard in trash. Larger quantities shall carefully take into consideration applicable DEA, EPA, and FDA regulations. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged, and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.

Synthesis of Chloramphenicol from 1,3-diacetylchloramphenicol
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Paraxin pentamycetin Quemicetina rivomycin romphenil Septicol sificetina Sintomicetina Sintomicetine R sintomicetiner Stanomycetin synthomycetin Synthomycetine Tevcocin thylacetamide tifomycin Tifomycine Treomicetina u-6062 Unimycetin veticol chlorocidinc chlorocidinctetran chlorocids Chlorocol Chloroject L chlorojectl Chloromax chloromycetny Chlorovules Cidocetine Ciplamycetin Cloramficin Cloramicol Cloramidina cloroamfenicolo Clorocyn Cloromisan Clorosintex halomycetin hortfenicol I 337A i337a Intramycetin isicetin Ismicetina isophenicol ,[theta-(theta,theta)]- [R-(R*,R*)]-2,2-dichloro-N-[2-hydroxy-1-(hydroxymethyl)-2-(4-nitrophenyl)ethyl]ethanamide 2,2-dichloro-n-(2-hydroxy-1-(hydroxymethyl)-2-(4-nitrophenyl)ethyl)-acetamid 2,2-dichloro-N-[2-hydroxy-1-(hydroxymethyl)-2-(4-nitrophenyl)ethyl]-,[R-(R*,R*)]-Acetamide 2,2-dichloro-n-[2-hydroxy-1-(hydroxymethyl)-2-(4-nitrophenyl)ethyl]-acetamid Acetamide, 2,2-dichloro-N-(beta-hydroxy-alpha-(hydroxymethyl)-p-nitrophenethyl) Acetamide, 2,2-dichloro-N-[2-hydroxy-1-(hydroxymethyl)-2-(4-nitrophenyl)ethyl]-, [R-(R*,R*)]- Acetamide, 2,2-dichloro-N-[beta-hydroxy-alpha-(hydroxymethyl)-p-nitrophenethyl]-, D-threo-(-)- acetamide,2,2-dichloro-n-(beta-hydroxy-alpha-(hydroxymethyl)-p-nitrophenethy Acetamide,2,2-dichloro-N-[2-hydroxy-1-(hydroxymethyl)-2-(4-nitrophenyl)ethyl]-,[R-(R*,R*)]- Alficetyn