Tigapotide (also known as PCK3145) is a synthetic peptide that is derived from the natural sequence of amino acids of the prostate secretory protein (PSP94), one of three predominant proteins found in human seminal fluid. PSP94 expression in the prostate is downregulated in patients with advanced prostate cancer and believed to be a survival mechanism for the cancer cells. Tigapotide can exert anticancer activity not only on prostate but also on breast and colon cancer cells, possibly through laminin receptor-mediated activation of MEK and ERK1/2 phosphorylation. However, the exact molecular mechanisms of action of Tigapotide against prostate cancer tumor growth and metastasis, and tumor-associated angiogenesis remain poorly understood. In preclinical trials, Tigapotide shows potent anticancer activity and reduces prostate cancer growth in PC3 xenograft mouse model and the Dunning rat R-3327 MLL model. Phase II a clinical trial results with Tigapotide confirmed its therapeutic safety and tolerability for metastatic hormone-refractory prostate cancer. This effect was in part correlated to a marked reduction in the high levels of plasma MMP-9, a gelatinase B enzyme involved in extracellular matrix degradation and tumor invasion, of patients receiving Tigapotide, suggesting a biological effect possibly related to control metastasis.

Semparatide (previously known as RS-66271) was developed as an analog of parathyroid hormone-related protein (PTHrP) with shortening the time for fracture healing. Experiments on animals have shown that this compound was an effective therapy for preventing impaired bone healing caused by prednisone. Clinical trials with postmenopausal osteoporotic women have revealed that semparatide cause sustained increases in the spine. However, further, development appears to have been discontinued by Roche.

CK-101 is an orally available third-generation and selective inhibitor of certain epidermal growth factor receptor (EGFR) activating mutations, including the resistance mutation T790M, with potential antineoplastic activity. Activating mutations in the tyrosine kinase domain of EGFR are found in approximately 20% of patients with advanced Non-Small Cell Lung Cancer (NSCLC). Compared to chemotherapy, first-generation EGFR inhibitors significantly improved ORR and progression-free survival in previously untreated NSCLC patients carrying EGFR mutations. However, tumor progression could develop due to resistance mutations, often within months of treatment with first-generation EGFR inhibitors. CK-101 designed to be highly selective against the T790M mutation while sparing wild-type EGFR, thereby improving tolerability and safety profiles. Compared to some other EGFR inhibitors, CK-101 may have therapeutic benefits in tumors with T790M-mediated drug resistance. This agent shows minimal activity against wild-type EGFR (WT EGFR) and does not cause dose-limiting toxicities that occur during the use of non-selective EGFR inhibitors, which also inhibit WT EGFR.