Our co-founder Dr. Anna Marie Pyle from Yale University is the co-discoverer of the RIG-I receptor family and conducted many of the key structural and biochemical investigations to understand the structure and function of RIG-I

RIG-I acts like a switch, remaining in its inhibited state in the cytosol until it encounters a high affinity RNA agonist which causes it to undergo a conformational change.

RIG-I is key to our natural defense against viral infection. When viral RNA enters our cells. It stimulates a rapid, natural defense response: activation of sensor proteins that trigger our “innate immune system”.

What Differentiates Our Approach from Other Strategies?

Differentiation of SLRs as Anti-Virals

  • Host-targeted mechanism
    • RIG-I agonists will not elicit antiviral resistance unlike DAAs
  • Pan-viral:  Broadly effective against existing and emerging RNA viruses
  • Selectively stimulated by specific viral mimics
  • Effective against variants and & drug resistant viruses

Differentiation of SLRs in anti-tumor capability

  • Advantages of targeting RIG-I vs. other PRRs (STING, TLR)
    • RIG-I is ubiquitously expressed in a variety of tumor cell types
    • RIG-I activation stimulates a strong interferon (type 1) response with induction for pro-inflammatory cytokines
    • RIG-I agonism provides a unique dual pronged strategy for anti-tumor effect involving a combination of immunogenic cell death of tumor cells and CD8+ T cell-mediated tumor cell apoptosis
    • RIG-I rarely mutates, reducing risk of resistance to treatment
    • Activation of innate immune system converts “cold” tumors to “hot”