Background: Cantharidin has been categorized as highly toxicant in Chinese medicine. But
cantharidin can efficiently treat different types of diseases, such as molluscum contagiosum. While
cantharidin is quite useful, unfortunately, due to its side effects, increasing regulations have limited
access to this useful therapeutic option. Cantharidin's toxic effects have caused it to fall into disuse for
most legitimate medical purposes. Although cantharidin generates effects and its advantages must be
realized. Recently, cancer affects people’s life more and more. Because cantharidin can treat some cancers,
so solutions must be used to reduce side effects. This review aims to describe some its analogues,
several efficient methods to inhibit the side effects of cantharidin and pharmacogenomics of cantharidin.
Methods: We searched for research about cantharidin by entering the database. Then evaluated these
papers and analyzed their founding, solution, mechanism, etc., and targeted to screen the papers related
to the content of our research, and then sorted them out in accordance with the solution, mechanism
research and other content. Finally, these content was unified into a framework.
Results: Some cantharidin's analogues were found that they show some similar functions to cantharidin
and we found that norcantharidin, acylthiourea derivatives, cantharidinamides, anhydride-modified
derivatives and other derivatives have less side effects. The modified cantharidin analogues reduce
toxicity in hepatocytes. Cantharidin consists of a six-ring and a five-ring, the moiety of oxygen on the
six-ring and the anhydride section exhibit biochemical activity. Protein phosphatases are associated
with many cellular processes including apoptosis, cell cycle progression and so on. Cantharidin can
cause apoptosis and double-stand breakage of DNA. Cantharidin and norcantharidin can efficiently
inhibit the activity of mammalian and plant protein phosphatase 1 (PP1) and protein phosphatase 2A
(PP2A) in vivo. Cantharidin inhibits PP5 at the nanomolar level with an IC50 value of 600 nM. PP5 can
manage the cellular survival, death, proliferation and other some intracellular biological activities in
mammals. After cantharidin’s treatment, the level of EtPP5 mRNA expression was downregulated.
Their also can be used to inhibit the Glutathione S-transferases (GSTs), angiogenesis and the expression
of A549 human lung cancer cells, trigger eryptosis and induced bladder cancer cell apoptosis. We
found that using Vitamin C and ginsenosides and translating cantharidin into nanoparticles can minimize
the cantharidin side effects in the patients.
Conclusion: Cantharidin can inhibit various tumor cell lines. Cantharidin causes both DNA single- and
double- strand breaks and induces apoptosis. Although cantharidin shows some toxicity for human, its
anti-cancer effects should be taken seriously. Several viable methods can help solve this problem. The
most important pharmacogenomics of cantharidin is that cantharidin can inhibit PPs, because PPs are
associated with many cellular processes. This prospect is very broad and needs to continue studying.