Technology

Our novel agent, the empty SV40 capsid, is composed of a single protein and does not contain any genetic material. This natural agent responds to a wide array of malfunctions in the organism. 

Wild type SV40 was declared by the NIH to be “non-pathogenic to human individuals” (https://osp.od.nih.gov/wp-content/uploads/NIH_Guidelines.pdf). All the more so for the empty capsids, which do not contain any genetic material and cannot propagate. 

Below is a high resolution, molecular model of the wild type virus and the empty capsid, solved by our group based on small angle X-ray scattering.

Wild Type SV 40 Empty capsid (NC)

Wild Type SV 40 - Empty capsid (NC)
The capsid proteins are shown in green, the DNA in blue and the nucleosomes (proteins which serve as scaffolds for the DNA) in red.

The NC treatment is a paradigm shift at several levels for the treatment of diseases with complex pathology:

  1. The NCs modulate gene expression profile of the host leading to activation of numerous pathways that promote tissue repair and recovery.
  2. The NCs affect different genes in different diseases, responding to the respective pathophysiology. 
  3. The NCs induce broad host anti-microbial defense mechanisms, unlike antibiotics that directly kill pathogens and contribute to the rise of drug resistant bacteria.
  4. The elicited signaling pathways become modified with time, adjusting to the recovery process of the treated animals.
  5. The NCs have a negligible effect on healthy animals, suggesting negligible side effects in clinical applications.  

These properties taken together indicate that the NCs bring the sick body to homeostasis – a balance of its physical, chemical and biological state.

In different experiments using animal models we show that: 

  • The survival of rats inflicted with severe sepsis and pre-treated with NCs is 75%, while all the rats that received placebo died within 4 days (Ben-Nun-shaul et al, 2020, Oncotarget 11:574-588). 
  • Pre-treatment with NCs increased survival of animals with acute kidney injury (AKI) induced by mercury poisoning (Butin-Israeli et al, PLoS ONE Aug 20;3(8):e2998)_and by the cancer drug cis-platinum (unpublished).
  • In rats inflicted with traumatic brain injury (TBI), post treatment with NCs improved brain function, suggesting that pre-treatment is not an inherent requirement of NC therapy (unpublished). 

Application     

  • Sepsis – current focus – data obtained from studies in a rat model (Ben-Nun-shaul et al, 2020, Oncotarget 11:574-588).
  • Acute kidney injury (AKI) – efficacy demonstrated in two mouse models: (mercury-induced AKI (Butin-Israeli et al, 2008, PLoS One Aug 20;3(8):e2998) and cis-platin induced AKI (unpublished). 
  • Traumatic brain injury (TBI) – preliminary study demonstrated recovery of brain damage in mice (unpublished).