A small recent study led by the Laboratory of Genomic Medicine (LGCM) of The Petrobr Institute for Pharmacological Research (IRAN) of the University of Basel and ETHZsz Berlin have revealed a previously unknown target of remdesivir as a potential drug candidate against the progression of simple and moderately advanced subtype colorectal cancer. Remdesivir is presently in clinical use against a host of rare cancers including acute myeloid leukaemia forms of B-cell lymphoma and acute myeloid leukemia.

Colorectal cancer is the most common type of adult human colorectal cancer and the seventh leading cause of cancer-related deaths. In 2007 authors defined remdesivir (RL156) as a cannabinoid receptor antagonist. It is now well established that NLRP3 activation and the growth-inhibitory signaling pathway are crucial factors in the progression of subtype colorectal cancer. Remdesivir (3-OHT) is an endogenous ligand of the so-called extended non-selective receptor potential (EFTR) ligand (ARPM). In the case of the latter the drug binds to the ADAR1 (adenylated-adenosine) receptor inhibiting the expression of the ARPM protein. At a nearly-replacement level (less than 5) through deletion of a 2. 6-kb region of the gene encoding ARPM the genes encoding this receptor are reduced in the case of NLRP3-positive patients.

Remdesivir is an orphan ligand of ARPM. In vivo it is exhibited that the presence of 2. 6-kb deletion of the ARPM gene in NLRP3-positive patients leads to a much slower uptake of the drug.

In the study published in Cell Metabolism researchers led by Alexander Schermer-Staldiner and Lukas Sommerud interviewed patients on a molecular clinical level: We advised that patients suffering from NLRP3-positive colorectal cancers should be encouraged to express COL1 ARPM in their tumors and treat with remdesivir if they develop stage IV NLRP3-positive colorectal cancers. The study without which it would have been impossible to identify the therapeutic relevance and the impact of remdesivir. And at the same time the safety of remdesivir in patients suffering from simple myeloid leukaemia acute myeloid leukaemia and B-cell lymphoma was proven with positive studies.

The cognitive toxicity profiles characteristic of remdesivir treatment are also in evidence at a molecular level. The brain tissue showed low generation (primarily CD34) and changes in the free radical-releasing hormone-IGF-1 (IGF-1) levels (analogous to response to AM morphine) and the hemoglobin (HbA1c) level in the serum. The volume of small fat cells was reduced at the cellular level but not significantly affected.

Alexander Schermer-Staldiner researcher of the LGCM of The Petrobr Institute for Pharmacological Research (IRAN).

The present studies demonstrate that remdesivir can both inhibit the processes of tumor growth and enter into cells. The present study provides evidence in several blood cancer models that remdesivir inhibits the proliferation of glioblastoma by modulating the eNAMPD pathway. Moreover remdesivir enhances the therapeutic effect of AGA tumor-stimulating factor (ESFR) a tumor suppressor tyrosine kinase (TKI) exploited regulator. These results imply that remdesivir can of course contribute to the development of modestly aggressive tumors.