(Sulfonamides and Related Drugs)

Copyright, Purdue Research Foundation, 1996

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Structure and chemical characteristics

Mechanism of action

Concentration Required to Inhibit DHFR by 50%
DRUGRAT LIVERE. coliP. berghei
IC50 (nM)IC50 (nM)IC50 (nM)
GG 8th, p985. Original data from Ferone, Burchall & Hitchings, 1969


Sulfonamide Pharmacokinetics

Dose forms



Sulfonamide Adverse Reactions



Direct toxicity


Renal crystalluria

Keratitis sicca

Decreased Thyroid Function


Cardiovascular collapse

Tissue necrosis

Blood dyscrasias


Drug interaction

Clinical Applications Sulfonamides

Trimethoprim Pharmacokinetics

Adverse Effects Trimethoprim

Clinical Application of Trimethoprim



Study Questions

  1. You should be able to name and discuss how the sulfonamides combined with trimethoprim exemplify three general mechanisms of drug action. What is the basis of selectivity in each of these mechanisms?
  2. Why are the sulfonamides and trimethoprim synergistic? Does their combination change their action from being bacteriostatic to bactericidal?
  3. How reasonable would it be to switch from one sulfonamide to another in therapy of an organism that is resistant to the first? Note that in vitro sensitivity testing of the sulfonamides is often misleading. Some authorities claim MICs derived from such tests often underestimate the concentration truely needed.
  4. How does the spectrum of activity of sulfonamides compare to that of the tetracyclines?
  5. Is the distribution of newer, systemic sulfonamides and trimethoprim similar to that of chloramphenicol? If so, why might the apparent Vd of a sulfonamide like sulfamethoxazole be so low?
  6. Why do pharmacists nearly always encourage patients to drink a lot of water when taking sulfonamides?
  7. Why does alkalinization of urine (what could you use?) enhance elimination and safety of sulfonamides?
  8. How do the "Law of Independent Solubility", additive antibacterial action, and "triple sulfas" related to each other? What place did these occupy in the history of sulfonamide use?
  9. How likely is one to use an oral dose form to treat a pneumonia caused by Pneumocystis carinii in patients with AIDS? What rule was presented earlier in the course that might speak to this issue?
  10. Name a couple of drugs with which the sulfonamides might interact and explain the basis of the interaction. Include two categories (mechanisms) of interactions. Examples: Protein binding and kernicterus; renal secretion and competitiors; cidal/static considerations.
  11. Why are sulfonamides generally not given by IM injection?
  12. Is it likely that sulfasalazine acts solely or primarily as an antibacterial? Give a reason for your conclusion.
  13. Under what conditions might one consider using sulfadoxine plus pyrimethamine as an antimalarial?
  14. What are the major adverse effects of the sulfonamides?
  15. Note that Primor[R] is a q1d "potentiated" sulfa that is equivalent to Tribrissen[R]. Ormetoprim is the pyrimidine in Primor[R] whereas trimethoprim is in Tribrissen[R].

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Gordon L. Coppoc, DVM, PhD
Professor of Veterinary Pharmacology
Head, Department of Basic Medical Sciences
School of Veterinary Medicine
Purdue University
West Lafayette, IN 47907-1246
Tel: 317-494-8633Fax: 317-494-0781

Last modified
9:34 PM on 4/29/96