Aminoquinuride (Surfen) binds to glycosaminoglycans (GAGs) and has been shown to influence their function, and the function of proteoglycans (complexes of GAGs linked to a core protein). Surfen was first described in 1938 as a component of depot insulin; however, subsequent studies have revealed its efficacy in binding to glycosaminoglycans (GAGs). Surfen contains four quinoline rings that contain positively charged amino or methyl groups. Surfen was found to bind with greatest avidity to heparin. There are now a handful of studies on the biological effects of surfen, many of which relate to its ability to block the interaction between GAGs and signaling proteins, including effects on growth factors (fibroblast growth factor and vascular endothelial growth factor) and fibrils associated with the binding of human immunodeficiency virus (HIV)-1 to target cells. Surfen inhibits the action of SEVI (semen-derived enhancer of HIV viral infection). Because SEVI can increase HIV infectivity by several orders of magnitude, supplementing current HIV microbicide candidates with SEVI inhibitors, such as surfen, might greatly increase their potency. Surfen has also been shown to reduce inflammation but inhibits remyelination in murine models of multiple sclerosis.

Exisulind (tentative trade name Aptosyn) is an antineoplastic agent, which was originally developed by Cell Pathways. This drug is an inhibitor of phosphodiesterase (PDE) isozymes: PDE5 and PDE4. Inhibition of PDE5 appears to be pharmacologically relevant, which leads to increase cGMP and activate protein kinase G at doses that induce apoptosis, whereas cyclic AMP levels were not changed. Exisulind has been in phase III clinical trials for the treatment of Non-Small Cell Lung Cancer and for the treatment of polyps in patients who have familial adenomatous polyposis (Colorectal Cancer and Small Intestine Cancer). In addition, this drug was in phase II/III for the treatment of Prostate Cancer, however, there studies have been discontinued.

Talmapimod is a p38 MAPK kinase inhibitor that inhibits p38 alpha with IC50 value of 9 nM which is 10-times lower then IC50 for p38 beta. Talmapimod was under clinical development for the treatment of Myelodysplastic Syndromes, Multiple Myeloma and Rheumatoid Arthritis (phase II), however, it seems to be discontinued as no longer presents in Janssen's pipeline.

Crolibulin is a tubulin-disrupting agent, interacting at the colchicine-binding site, developed by EpiCept Corporation (which was later acquired by Immune Pharmaceuticals). The compound exhibits anti-cancer effect by vascular disruption and inhibition of apoptosis. In preclinical animal tumor models, combination therapy with crolibulin has demonstrated the synergistic activity with cytotoxic drugs as well as anti-angiogenic drugs, such as Avastin. The drug was investigated in clinical trials for the treatment of anaplastic thyroid cancer and has demonstrated a positive effect.

Tianafac (also known as L8109) is a thienylacetic acid derivative patented by Labaz group as antipyretics and anti-inflammatory agent useful for the treatment of arthritis. In preclinical models, Tianafac inhibits prostaglandin formation by seminal vesicle microsomes and exerts antipyretic, analgetic, and moderate gastric ulcerogenic activity and had a wide safety margin between toxic and pharmacologically active doses.

Nicaraven is a hydroxyl radical scavenger with antivasospastic and neuroprotective effects. Chugai (the Japanese subsidiary of Roche) is developing nicaraven (Antevas), a water-soluble antioxidant, for the potential treatment of disorders caused by acute cerebrovascular diseases. A registration application was filed in April 1995, and in April 2002, nicaraven was still awaiting registration in Japan. By August 2002, Chugai had filed an NDA in Japan for the additional indication of subarachnoidal bleeding.

Gedatolisib (PF-05212384, PKI-587) is a highly potent dual inhibitor of PI3Kα, PI3Kγ and mTOR, originally being developed by Wyeth. Upon intravenous administration, gedatolisib inhibits both PI3K and mTOR kinases, which may result in apoptosis and growth inhibition of cancer cells overexpressing PI3K/mTOR. Activation of the PI3K/mTOR pathway promotes cell growth, survival, and resistance to chemotherapy and radiotherapy; mTOR, a serine/threonine kinase downstream of PI3K, may also be activated independent of PI3K. Significant antitumor efficacy and a favorable pharmacokinetic/safety profile justified clinical evaluation of Gedatolisib. Gedatolisb is in phase II clinical trials by Pfizer for the treatment of acute myeloid leukaemia. Gedatolisb is in phase I clinical trials for the treatment of solid tumours.

Mefeclorazine is a non-steroidal anti-inflammatory drug. It inhibits prostaglandin synthesis.

Lunacalcipol (CTA-018 or MT-2832) is a vitamin D analog having a dual mechanism of action. It inhibits CYP24A1 and induced VDR expression. It was being developed for the treatment of clinical consequences of vitamin D insufficiency and secondary hyperparathyroidism associated with chronic kidney disease. Lunacalcipol development has been discontinued.