Ridaforolimus (Deforolimus, MK-8669) is an investigational oral mTOR inhibitor in development for the treatment of metastatic soft-tissue or bone sarcomas. Ridaforolimus is being co-developed by Merck and ARIAD Pharmaceuticals. Ridaforolimus (Deforolimus, MK-8669) is a selective mTOR inhibitor with IC50 of 0.2 nM in HT-1080 cell line; while not classified as a prodrug, mTOR inhibition and FKBP12 binding is similar to rapamycin. mTOR is a protein kinase that controls cell growth by regulating many cellular processes, including protein synthesis and autophagy. Compared with other mTOR inhibitors, ridaforolimus is not a prodrug and has shown in vivo stability. Both intravenous and oral formulations of the compound are being tested in clinical trials for the treatment of various solid tumors and hematologic malignancies. The initial indication is soft-tissue and bone sarcomas. Ridaforolimus was indicated to treat patients with metastatic soft tissue sarcoma or bone sarcoma whose disease has not progressed after at least 4 cycles of chemotherapy. In June 2012, Merck & Co., Inc. announced the receipt of a Complete Response Letter from the U.S. Food and Drug Administration (FDA), advising the company that the New Drug Application (NDA) for ridaforolimus had not been approved. Currently Ridaforolimus is in phase III clinical trials for the treatment of Coronary artery restenosis.

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).