Modimelanotide is a melanocortinergic peptide drug derived from α-melanocyte-stimulating hormone (α-MSH) which was under development for the treatment of acute kidney injury. Modimelanotide had promising preclinical data, and a Phase II trial in patients undergoing cardiopulmonary bypass surgery showed a reduced incidence of acute kidney injury in subjects that received Modimelanotide. However, a Phase IIb, multicenter study of Modimelanotide in patients with chronic kidney disease who underwent cardiopulmonary bypass surgery failed to show a significant reduction in the incidence of acute kidney injury in subjects who received the drug, both by serum creatinine measurements and by novel biomarkers of tubular injury.

Detirelix is a synthetic decapeptide containing five D-amino acids. It is a very potent Gonadotropin-releasing hormone (GnHR) antagonist. The acute effects of detirelix were consistent with peripheral vasodilation. Subchronic effects were associated with inhibition of pituitary gonadotropic and gonadal hormone secretion. As long-acting GnRH antagonist detirelix can rapidly suppress gonadotropin secretion, inhibit follicular development, and prevent ovulation. It can be used as luteolytic agent. A projected use is for the treatment of sex hormone-releasing diseases, as part of anticancer hormone therapy of sex-hormone-dependent tumors.

ABT-510 is an anti-angiogenesis compound that was under development by Abbott for the treatment of solid tumours, lymphoma and melanoma. It is a synthetic peptide that mimics the anti-angiogenic activity of the endogenous protein thrombospondin-1 (TSP-1). ABT-510 inhibits the actions of several pro-angiogenic growth factors important to tumor neovascularization; these pro-angiogenic growth factors include vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF)), hepatocyte growth factor (HGF), and interleukin 8 (IL-8).

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.