MECHANISM OF ACTION

ANTI-INFECTIVES

Etylene Oxide- Non-Alkylating Agent (Carcinogenic)

Aldehydes- direct and non-specific alkylation of the nucleophilic functional groups of proteins and
nucleic acids forming carbinols.

Phenols- acts on cell membrane and inactivates intra-cytoplasmic enzymes forming unstable complexes.

Oxidizing Agents- liberation of oxygen and denatures proteins.

Iodine- protein inactivation by iodination of phenylalanyl and tyrosyl residues; oxidation of -SH groups.

Hydrous Benzoyl Peroxide- induce proliferation of epithelial cells leading to sloughing and repair.

Chlorine- chlorination (oxidation) of amide nitrogen (peptide bond) atoms in protein and oxidation of
sulfhydryl groups.

Cationic Surfactant- lower down the interfacial tension *

Nitromersol- formation of covalent compounds.

Elemental Mercury- reacts with the -SH of enzymes and the other proteins by forming R-S-Hg-R

ANTI-FUNGALS

Phenols and derivatives- interfere the cell membrane integrity and function in the susceptible fungi.

Ciclopirox olamine- Low concentration: block the amino acids into the cell; high concentration: lost of
membrane integrity and cellular constituents.

Flucytosine- inhibits thymidylate synthetase.

Polyenes- inhibits ergosterol

Griseofulvin- mitotic spindle poison, binds to the tubulin dimes required for microtubule assembly.

Allylamines and related compounds- inhibits squalene epoxidase.

Azoles-inhibits lanosterol.

Clotrimazole- interferes with the amino acid transport into the organism by an action of CM.

Aureobasidins- noncompetitive inbihitor of inositol phosphorylceramide sphingolipid biosynthesis.

Echinocanadins and Pneumocanadins- noncompetitive inhibitor of 1,3-B-d-glucan synthase.

Quinolones- inhibits of DNA Gyrase.

Nitrofurans- reduction (nitrofuran reductase) of the nitro group coupled with the formation of free
radicals (reactive intermediates) which cause the damage of ribosomal proteins especially the DNA,RNA,
protein, and cell wall synthesis. Overall inhibition of cell growth or cell death.

Methenamine- liberation of formaldehyde and enhanced by acidifying the sodium biphosphate or

ammonium chloride.

ANTI-PROTOZOALS

Metronidazole- enters bacteria via cell diffusion.

Eflornithine- inhibitor of ornithine decarboxylase.

Dimercaprol- chelation

ANTHELMINTHICS

Piperazine-increase the resting potential of the helminth muscle so that the muscle membrane is
supressed leading to flaccid paralysis.

Pyrantel pamoate- promotes depolarization of the helminth’s myoneural junction and cholinesterase
inhibition.

Mebendazole- inhibition of glucose uptake leading to depleted glycogen storage-> decrease ATP
synthesis.

Niridazole- inhibits the conversion of the active form schistosomal glycogen phosphorylase into inactive
form.

Niclosamide- inhibition of glucose uptake, inhibition of energy production by anaerobic metabolism and
inhibition of inorganic phosphate incorporation into ATP.

Praziquantel- produce tetanic-like contraction within the muscle system of the fluke leading to the
segment of worms.

SULFONAMIDES- inhibits dihydropteroate synthase

Sulfamethoxazole- inhibits dihydrofolate synthase.

Trimethoprim- inhibits dihydrofolate reductase.

Sulfones- same as sulfonamides.

ANTI-MALARIAL

Doxycycline- inhibits protein synthesis.

Lumefantrine- inhibition of B-hematinin by forming complex with hemin.

Sulfadoxine + Pyrimethamine- inhibition of folic acid biosynthesis and dihydrofolate reductase.

Primaquine- disruption of parasites mitochondria.

Atovaquone and Proguanil- inhibition of dihydrofolate reductase and damage to the parasites
mitochondria.

Artemether and lumefantrine- inhibition of non-mevalonate pathway.

Fosmidomycin- inhibition of glutathione reductase.

ANTI-NEOPLASTIC

Orgaplatinum- establishes cross-links within and between DNA strands.