Our Science and Innovation
D3 Science is pleased to introduce our line of SafeSweet and SafeSpray antiviral products. We have recognized the fear and uncertainty that has crippled America, bankrupted untold numbers of small and mid-sized businesses, and has crushed many entrepreneurial dreams. We stand behind our products, through extensive literature review, numerous rounds of laboratory testing, and limited testing in human subjects, we believe that the SafeSweet and SafeSpray line of products can impact the ability of SARS-CoV-2 spike protein from binding to mucosal tissue.
Inhibiting the binding also referred to as fusion, and subsequent cellular uptake of a virus is a mechanism of action employed by several Food and Drug Administration (FDA) approved medications as well as numerous investigation medications used to treat viral borne diseases ranging from HIV-1 to Dengue Virus. (1,2). One important distinction needs to be made, particularly to HIV-1. Those medications do not prevent viral infection. Our products are designed to be used prophylactically to greatly reduce the ability of the spike protein to bind to mucosal tissue.
The SARS-CoV-2 envelope is studded with spike proteins which bind to certain cell surface receptors on mucosal epithelial tissue. Unfortunately for humans, these spike proteins match up like a lock and key, if you can visualize that model, the cell surface receptors represented by the lock and the spike protein thus the key. If one would alter the key, or block the lock, the virus cannot enter the cell. The ACE-2 receptor is the most likely epithelial tissue cell surface receptor for the SARS-CoV-2 virus (3). The most current literature also suggest the presence of the neurophilin-1 (nrp-1) receptor having an important role in the virulence of the virus (4).
We have formulated our products with compounds the FDA has designated as generally regarded as safe (GRAS). SafeSweet products include a hard candy delivery system. SafeSpray includes both an oral and nasal spray. Through in vitro testing with human mucosal epithelial cells we have confirmed a clinically significant reduction in the binding of spike protein. By blocking theses main sites of viral-cell interactions we believe our products will reduce the ability of the SARS-CoV-2 spike protein to bind to mucosal epithelial tissue. Our compounds effectively block the main fusion sites of the virus by, to use the above analogy, altering both the key (spike protein) but also the lock (ACE-2 and nrp-1).
We believe that the distribution of a vaccine could be extensive. Our testing not only confirms the existing literature but allows us the procedures to validate raw materials, providing standardization in a market plagued with substandard and untested products.
1. Venanzi Rullo, E., Ceccarelli, M., Condorelli, F., et al.”Investigational drugs in HIV: Pros and cons of entry and fusion inhibitors (Review)”. Molecular Medicine Reports 19.3 (2019): 1987-1995.
2. De La guardia, Lleonart R. Progress in the Identification of Dengue Virus Entry/Fusion Inhibitors. BioMed research International. Vol 2014. https://doi.org/10.1155/2014/825039
3. Yang, J., Petitjean, S.J.L., Koehler, M. et al. Molecular interaction and inhibition of SARS-CoV-2 binding to the ACE2 receptor. Nat Commun 11, 4541 (2020). https://doi.org/10.1038/s41467-020-18319-6
4. Cantuti-Castelvetri L , Ojha R, Pedro LD. et al. Neuropilin-1 facilitates SARS-CoV-2 entry and infectivity. Science 20 Oct 2020. https://doi.org/10.1126/science.abd2985