Rifampin

Anti-tuberculosis Drug
Parimala G, 17303007
 Tuberculosis, affecting the world’s poorest populations, remains
one of the biggest public health problems in the 21st century
 Presently, one-quarter of the world's population is thought to be
infected with TB
  Number one cause of death from an infectious disease
 More than 95% of deaths occurred in developing countries,
around 1 million cases per year (India)
 Recommended treatment of new-onset pulmonary tuberculosis -
six months of a combination of antibiotics containing rifampicin,
isoniazid, pyrazinamide, and ethambutol for the first two
months, and only rifampicin and isoniazid for the last four
months
Pharmacologic agents for treatment of tuberculosis
(TB) are utilized in a hierarchical fashion
First line of agents
 ethambutol is EMB or E,
 isoniazid is INH or H,
 pyrazinamide is PZA or Z,
 rifampicin is RMP or R,
 streptomycin is SM or S

Second line of agents

 fluoroquinolones (notably levofloxacin and moxifloxacin),
 injectable-only agents (such as aminoglycosides and
capreomycin)
Rifampin  Bactericidal antibiotic drug of the rifamycin group 1
 Semisynthetic compound derived from Amycolatopsis rifamycinica
 A polyketide belonging to the chemical class of compounds termed 
ansamycins
 Rifampin is a red-brown crystalline powder very slightly soluble in
water at neutral pH, freely soluble in chloroform, soluble in ethyl
acetate and in methanol. Its molecular weight is 822.95 and its
chemical formula is C43H58N4O12.

Trade Rifampicin; Rifampin; Rifadin; Rimactane; Rimactan;

Name: Rifamycin
 (7S,9E,11S,12R,13S,14R,15R,16R,17S,18S,19E,21Z)-2,15,17,27,29-pentahydroxy-11-
IUPAC
methoxy-3,7,12,14,16,18,22-heptamethyl-26-[(1E)-[(4-methylpiperazin-1-
Name:
yl)imino]methyl]-6,23-dioxo-8,30-dioxa-24-azatetracyclo[23.3.1.1⁴,⁷.0⁵,²⁸]triaconta-
1(29),2,4,9,19,21,25,27-octaen-13-yl acetate

The critical functional groups of rifampicin in its inhibitory binding of bacterial RNA
polymerase are the four critical hydroxyl groups of the ansa bridge and the napthol ring, which
form hydrogen bonds with amino acid residues on the protein
Pharmacokinetics
Pharmacokinetics
  Orally administered rifampicin results in
peak plasma concentrations in about 2-4
hours
 Rifampicin is easily absorbed from the 
gastrointestinal (GI) tract;
Pharmacokinetics  Only about 7% of the administered drug is
excreted unchanged in urine
 About 60% to 65% is excreted through feces
 The half-life of rifampicin ranges from 1.5 to
5.0 hours
DRUG INTERACTION
Ascorbic acid The serum concentration of Ascorbic acid can be increased when it
is combined with Rifampicin.

Calcitriol The metabolism of Rifampicin can be increased when combined

with Calcitriol.

Cholecalciferol The metabolism of Rifampicin can be decreased when combined

with Cholecalciferol.

Ergocalciferol The metabolism of Rifampicin can be decreased when combined

with Ergocalciferol.

Fish oil The metabolism of Rifampicin can be decreased when combined

with Fish oil.

Vitamin D The metabolism of Rifampicin can be decreased when combined

with Vitamin D.
  Multi-drug-resistant tuberculosis (MDR-TB) is a form of 
tuberculosis (TB) infection caused by bacteria that are resistant to
treatment with at least two of the most powerful first-line 
anti-TB medications (drugs), isoniazid and rifampin.
 Treatment of MDR-TB requires second-line drugs (i.e., 
Multi – Drug fluoroquinolones, aminoglycosides, and others), which in general are
Resistant less effective, more toxic and much more expensive than first-line
drugs
Tuberculosis:  If these second-line drugs are prescribed or taken incorrectly, further
resistance can develop leading to XDR-TB.
 Research: Much research and funding is needed in the diagnosis,
prevention and treatment of TB and MDR TB.
Recent
advancements
 Kanglemycin A (KglA) inhibits
rifampicin-resistant RNA
polymerases (RNAPs)
 KglA’s extra groups improve
binding to RNAP and block first
dinucleotide formation
 KglA is effective against
multidrug-resistant M.
tuberculosis
 • Kaplan, Jeffrey. 2017. "Tuberculosis" American University. Lecture.
• Nathanson, Eva; Nunn, Paul; Uplekar, Mukund; Floyd, Katherine;
Jaramillo, Ernesto; Lönnroth, Knut; Weil, Diana; Raviglione, Mario
(2010-09-09).
• "MDR Tuberculosis — Critical Steps for Prevention and Control". New

References: England Journal of Medicine. 363 (11): 1050–1058. doi:

10.1056/NEJMra0908076. ISSN 0028-4793. PMID 20825317.
• "Drug-resistant tuberculosis". World Health Organization.
Retrieved 2018-10-02.
• "Multi-drug-resistant tuberculosis (MDR-TB) – 2015 Update". WHO.
Retrieved 7 December 2016.
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