Abstract Futuristic Background



NTI-55: AR5/TR5 Nammisome

  • Formulation Lipid NanoParticle (LNP) with A2A receptor inhibitor prodrug (AR5) and Toll Receptor 7 agonist prodrug (TR5) incorporated.

  • AR5 rationale: A2A receptor has been clinically validated to be an important immune checkpoint. Inhibition of this receptor by the active component of AR5 and other inhibitors has demonstrated anti-tumor activity in the clinic.

  • TR5 rationale: Toll receptor 7 agonists are clinically validated to have anti-tumor activity but are generally too potent to give as free drugs. Incorporation of the prodrug in a Nammisome targets the activity to tumors while reducing systemic activity allowing for safe delivery of effective doses.

  • Target Indications: While the immune mechanisms targeted by AR5/TR5 are independent of cancer type, the mechanism of selective tumor delivery of Nammisomes is dependent on presence of a tumor mass (as opposed to dispersed cells). Therefore, solid tumors would be the potential market for this product. Initial development will be determined by done in multiple indications to demonstrate efficacy in a large indication such as breast cancer and in an indication with Orphan Drug Potential such as bladder, pancreatic, and renal cancers.


Mechanistic Validation of LNP-AR5/TR5

LNP-prodrugs are more potent than free drugs


NTI-55: Anti-Tumor Efficacy in Vivo

Efficacy in a Murine Model of Breast Cancer (EMT6)


NTI-55 Efficacy in Murine Colon Cancer Model (MC38)