LTX-315 has been de novo designed based on structure–activity relationship studies of host defense peptides. The oncolytic effect of LTX-315 involves a unique immunogenic cell death targeting the mitochondria with subsequent release of danger-associated molecular pattern molecules. This initial targeting of the mitochondria is followed by disintegration of other cytoplasmic organelles resulting in effective release of additional danger signals and a broad repertoire of tumor antigens and finally lysis of plasma membrane (necrosis).
Preclinical and clinical studies have demonstrated LTX-315`s unique ability to reshape the tumor microenvironment by inducing effective release of danger signals, chemokines and a broad repertoire of tumor antigens. These properties of LTX-315 results in enhanced infiltration of activated CD 8 T cells and Th1 responses.
This ability to convert non-T cell inflamed tumors to T cell inflamed tumors makes LTX-315 an ideal combination partner with other types of immunotherapy, including immune checkpoint inhibitors/agonists, vaccines and T cell based therapies.
Both preclinical and clinical studies have confirmed LTX-315s ability to induce systemic anticancer immune response when injected locally into tumors resulting in complete or partial regression of injected and non-injected tumors (i.e. abscopal effect). Preclinical studies have demonstrated strong synergy with immune-checkpoint blockade which have given the scientific rationale for initiating combinations studies with Ipilimumab and Pembrolizumab in melanoma and TNB cancer patients respectively.
LTX-315`s unique mode of action results in effective “release and reshape in the tumor microenvironment
LTX-315 is an oncolytic immunotherapy. Time lapse study with confocal microscopy shows that the human melanoma cell (A547) is killed within minutes by LTX-315. (Courtesy of L.M. Eike and B. Sveinbjørnsson, UiT)
Presentation of LTX-315 – the discovery and its mode of action