We helped pioneer the expansion of the use of TA

We helped pioneer the expansion of the use of Tranexamic Acid (TA) to the reduction of bruising and inflammation in cosmetic surgery and non-surgical procedures, working with Dr. Rod Rohrich (Rohrich & Cho, 2018). TA’s use to reduce bruising in non-surgical procedures is novel. We have developed an optimal gel-based product that is easier to use and allows a much higher concentration of TA.

Our development of TA as an antiviral agent is even more ground-breaking. Although TA is a lysine analog, we determined that it antagonizes not just lysine but also arginine and histidine, as all have a similar chemical structure. Since these are the three positively charged amino acids, we had the further insights that TA’s method of action involves interference with the electrostatic bond involved in numerous protein-protein and protein-DNA/RNA interactions, and that these are essential not just for viral replication but also for cancer growth and the development of many other diseases.

Our testing also indicated that TA can be combined synergistically with synthetic analogs of arginine and histidine, and development of those compounds is underway. Because of their similar structure and function, we have named these synthetic analogs the Tranexamic Class Antagonists (TXCAs) of positively charged amino acids.

The protein-protein electrostatic bonds involving lysine, arginine, and histidine residues are required for many fundamental activities, such as histone acetylation and methylation and nuclear localization. Our testing has shown that TA inhibits the translation of at least four different genes of HSV-1. For many viruses, cell attachment and entry also require involvement of the three positively charged amino acids. For example, the spike protein of SARS-CoV-2 is cleaved at a group of arginine residues by furin or plasmin, and its attachment to the ACE2 receptor and cleavage of the ACE2 receptor to enhance entry into the cell involve lysine, arginine, and histidine residues.

With respect to cancer and other diseases, our testing has shown that TA inhibits the activities of the general transcription factor p300, and we believe that TA will prove to be the first safe inhibitor of p300/CBP. The blood-related cancers and others that over-express MYC also appear to be particular targets.

We have tested TA successfully in vitro and in vivo against a variety of different viruses, and given its MOA we believe it is a very broad spectrum (possibly universal) antiviral agent. Its application as an anti-cancer agent should be similarly effective, and without the toxicity involved with most chemotherapies.

One of the fascinating things about TA, based on our research and that of others, is that it has several significant secondary effects that are extremely beneficial in inhibiting viral infection and the development of cancer and other diseases: it is anti-inflammatory, it enhances the innate immune response, it stimulates mitochondrial function, and it protects the epithelium. In addition, in over 50 years of use across a wide range of dosages and administration forms, it has shown to be extremely safe, with very few side effects. By its chemical structure, it cannot be incorporated into a protein, and it is very rapidly metabolized.

Because of TA’s multiple direct and secondary benefits and its unusual method of action that is unlikely to interfere with other drugs, it is an excellent candidate for combinations. The numerous benefits of drug combinations are listed in Areas of Focus.