The range of candida treatments ranges from time-proven and safe fatty acids, to dangerous drugs that create resistant strains, to obscure treatments like turpentine. With candida being an orphaned condition by the medical profession, many people take advantage of this void by selling anything they can to make a buck. While promising a quick cure, they put down everything and everyone else in an attempt to steer people away from following sound advise. Lufenuron is a good example of this trend. Designed and marketed as a flea medication for pets, at least two sites are trying to market it as a treatment for candida, in spite of the science that shows it doesn’t work against fungus.

Lufenuron is being pitched to candida sufferers as an effective anti-fungal due to its ability to act as a chitin synthesis inhibitor. Chitin makes up a good portion of the exoskeletons of insects and chitin inhibitors can cause this exoskeleton to break down. Chitin is also found in the cell wall of candida to varying degrees, depending on the environmental stresses that candida encounters. Unlike the exoskeleton of insects, candida has an ability to manipulate the chitin content in its cell wall membranes. If the environment that it finds itself in has chitin inhibitors, candida will alter its chitin content to preserve the integrity of its cell wall membrane. Sites that sell lufenuron would like you to think that candida doesn’t have this ability, which reveals a deep misunderstanding of how candida works.


Researchers from the University of California, San Francisco, decided to look at whether or not lufenuron had any anti-fungal effects. They found, “No evidence of inhibition, either by susceptibility testing or direct microscopic examination of treated cells, was obtained with lufenuron“. In contrast, they showed that a known chitin synthesis inhibitor, Nikkomycin Z, had a potent inhibitory effect against chitin in fungal cell wall membranes. Their conclusion –  “lufenuron does not appear to possess anti-fungal properties”.

Examining the scientific literature on lufenuron reveals other information that these sites fail to mention:

Lufeneron showed initial promise as a treatment for fungal infections, but the early enthusiasm has dampened considerably as efficacy appears doubtful.

Adverse effects reported in dogs and cats after oral lufenuron include: vomiting, lethargy/depression, pruritus/urticaria, diarrhea, dyspnea, anorexia, and reddened skin. The manufacturer reports that the adverse reaction rate is less than 5 animals in one million doses.

Of relevance to microbiology, chitin is present in fungal species such as mushrooms, where it can comprise from 5% to 20% of the weight of the organism.

Chitin synthesis inhibitors share a similar chemical structure as other benzoylphenyl ureas.Their mode of action is by interfering with the polymerization pathway of chitin, inducing accumulation of the monomer uridine diphospho-N-acetylglucosamine and blocking its synthesis (Beeman 1982). 

The final step  of  chitin  biosynthesis is  the polymerization of  N-acetylglucosamine from  the  activated  substrate  UDP-N-acetylglucosamine,  by  the  enzyme  chitin  synthase (EC  This enzyme has been well studied in fungi  and yeasts (Gooday 1977)…Leighton e t  al.  (1981)  have  proposed that diflubenzuron  acts indirectly  on  chitin synthase  by inhibiting a  proteolytic enzyme  required for its  activation from  the  zymogen form.

Lufenuron is a benzoylphenylurea drug that interferes with chitin synthesis. It is used in veterinary medicine as a flea prophylactic product, due to its non-specific inhibitory effect on chitin synthesisprobably related to serine protease inhibition


An unexpected result of lufenuron treatment was the inhibition of midgut epithelial cell differentiation. At concentrations of 0.5 and 1.0 ppm, partially differentiated epithelial cells were seen in the midgut of blood-fed fleas along with fully differentiated cells.

Micrographs of ovaries, from animals treated with lufenuron, showed some space between the follicular epithelium and the oocyte membrane. The in vivo incorporation of radioactive N-acetylglucosamine into chitin was inhibited by the presence of lufenuron.…

Potential Harm


Lufenuron bioaccumulates.

The studies above demonstrate that lufenuron can cause intestinal cell line damage and leaky gut. One benefit of the intestinal cells is that they regenerate quickly, thus demonstrating their ability to heal and restore the intestinal barrier. Lufenuron has the ability to block this regeneration. It’s role in serine protease inhibition could lead to chronic inflammatory conditions, food allergies, autoimmune diseases, etc.
Lufenuron can also interfere with absorption of N-Acetylglucosamine, necessary for the formation of the cell walls in many beneficial bacteria.

Disturbance of the epithelial barrier and epithelial transport processes is often discussed to be a major factor in the pathogenesis of intestinal inflammation and inflammatory bowel disease.

The intestinal epithelium provides a critical protective barrier against enteric pathogens, food antigens, and physiochemical stresses caused by digestive and microbial products, and yet must be selectively permeable to beneficial nutrients and fluids. Tightly regulated control of barrier function and integrity is critical, as the pathogenesis of intestinal diseases such as Crohn’s disease, ulcerative colitis, inflammatory bowel diseases (IBD), and autoimmune diseases are linked to intestinal barrier dysfunction and increased intestinal permeability (1). The intestinal epithelium is a single layer of linked columnar epithelial cells that regulates, through the paracellular pathway, the selective passage of ions, fluid, and macromolecules from the intestinal lumen into the underlying tissues.

The intestinal epithelium serves as a major protective barrier between the mammalian host and the external environment. Here we show that the transmembrane serine protease matriptase plays a pivotol role in the formation and integrity of the intestinal epithelial barrierSt14 hypomorphic mice, which have a 100-fold reduction in intestinal matriptase mRNA levels, d