LTX-315 is a cationic amphipathic peptide that preferentially permeabilizes mitochondrial membranes, thereby causing partially BAX/BAK1-regulated, caspase-independent necrosis. 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 ineffective release of additional danger signals and a broad repertoire of tumour antigens and finally lysis of plasma membrane (necrosis). Preclinical and clinical studies have demonstrated LTX-315`s unique ability to reshape the tumour microenvironment by inducing the effective release of danger signals, chemokines and a broad repertoire of tumour 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 tumours to T cell inflamed tumours 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 a systemic anticancer immune response when injected locally into tumours resulting in complete or partial regression of injected and non-injected tumours (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. Phase Ib study combining LTX-315 with ipilimumab (anti-CTLA4) in malignant melanoma patients, as well as LTX-315 with pembrolizumab (anti-PD-1) in metastatic breast cancer patients, is ongoing.