Albendazole binds to the colchicine-sensitive site of tubulin causes degenerative alterations in the tegument and intestinal cells of the worm, thus inhibiting its polymerization or assembly into microtubules. Because of loss of the microtubules leads to inhibition of glucose uptake by the larval and adult stages of the parasites, and depletes their glycogen stores. Degenerative changes in the endoplasmic reticulum, the mitochondria of the germinal layer, and the subsequent release of lysosomes result in decreased production of adenosine triphosphate (ATP), which is the energy required for the survival of the helminth. Due to diminished energy production, the parasite is immobilized and eventually dies. It is poorly soluble in water therefore shows poor absorption. Plasma protein binding is found to be 70%. Metabolised in liver and is excreted in bile with a half-life of 8 to 12 hours.

Ivermectin is a semisynthetic, anthelminitic agent and is a part of pentacyclic sixteen-membered lactone (i.e. a macrocyclic lactone disaccharide) derived from the soil bacterium Streptomyces avermitilis. Ivermectin binds selectively and with high affinity to glutamate-gated chloride ion channels in invertebrate muscle and nerve cells of the microfilaria. This binding causes an increase in the permeability of the cell membrane to chloride ions and results in hyperpolarization of the cell, leading to paralysis and death of the parasite. Ivermectin also is believed to act as an agonist of the neurotransmitter gamma-aminobutyric acid (GABA), thereby disrupting GABA-mediated central nervous system (CNS) neurosynaptic transmission. Oral absorption can be increased when taken with high fat meal and the volume of distribution is 3-3.5 L. Ivermectin shows 93% of the plasma protein and is mainly metabolised in liver. Metabolites are excreted in feces and the half-life is 16 hours.