SOR-C13, is a novel, short, synthetic peptide developed from the C-terminal region of soricidin, a proprietary 54 amino acid peptide, discovered by Soricimed Biopharma found in the saliva of the Northern Short-tailed Shrew. SOR-C13 binds with high affinity and selectivity - and disrupts the function of - TRPV6, a calcium channel over-expressed in solid tumor cancers. TRPV6 plays a central role in a biochemical cascade that results in the upregulation of an array of pro-cancerous genes. TRPV6 is considered to be an important target for novel anticancer therapy. SOR-C13 is the first highly specific TRPV6 inhibitor to be identified and to be taken into clinical development. SOR-C13 was effective in inhibition of tumors in animal xenograft models of human ovarian and breast cancer. The ongoing phase I trial studies the side effects and best dose of SOR-C13 in treating patients with solid tumors. The FDA has awarded orphan drug status to SOR-C13 for the treatment of ovarian cancer and for the treatment of pancreatic cancer.

Glaspimod (SK&F 107647) is a synthetic hematoregulatory peptide that shares biological and/or modulatory activities with natural hematopoietic cytokines. The peptide has been tested in vitro and in vivo for hematopoietic effects (involvement in production of cellular blood components). In vitro, glaspimod has no direct colony-stimulating activity (CSA), In vivo, injection of the compound results in an increase in serum CSA (maximal at 6 hours after injection). With repeated administration, significant increases in absolute numbers of granulocyte-macrophage (CFU-GM), erythroid (BFU-E), and multipotential (CFU-GEMM) progenitor cells can be measured. Pharmacokinetic effects of glasmipod have been studied in patients with adenocarcinoma and were not amenable to standard therapy.

LANCOVUTIDE, also known as duramycin, is a 19-amino-acid tetracyclic peptide antibiotic. It is in clinical development for the treatment of cystic fibrosis (CF). It activates an alternative chloride channel in lung epithelial cells by elevating intracellular calcium levels, and may potentially compensate for CF transmembrane conductance regulator deficiency in the airway epithelium and increase the volume of the airway surface liquid.