CI-201 (also known as VB-201) is pure synthetic Lecinoxoid, oxidized phospholipid analog, for prevention and treatment of atherosclerosis and central nervous system (CNS) autoimmune inflammatory disease. In preclinical models, CI-201 ameliorated the severity of experimental autoimmune encephalomyelitis (EAE) induced by myelin oligodendrocyte glycoprotein (MOG) peptide, and constrained the infiltration of pathogenic CD4+ T-cells into the CNS and impaired their IFN-γ production. CI-201 inhibits Toll-like receptor (TLR) signaling restricted to TLR-2 and TLR-4 in human monocytes and dendritic cells, and exhibits up to 90% inhibition of monocyte chemotaxis in vitro. Interestingly, CI-201 did not inhibit monocyte adhesion or phagocytosis and had no effect on chemotaxis of neutrophils. In vivo, oral treatment with CI-201 reduced monocyte migration in a peritonitis model and inhibited atheroma development in ApoE(-/-) mice, without affecting cholesterol or triglyceride levels. CI-201 is developed by Vascular Biogenics for the oral treatment of atherosclerosis, rheumatoid arthritis (RA), plaque psoriasis and multiple sclerosis (MS). However, in Phase 2 clinical trials CI-201 failed to demonstrate a statistically significant reduction in vascular inflammation associated with atherosclerotic lesions over placebo. As a result, Vascular Biogenics discontinued the development of CI-201 in psoriasis and atherosclerosis. No information about rheumatoid arthritis and multiple sclerosis clinical trials are currently available.

Ridogrel is a dual action drug used for the prevention of systemic thrombo-embolism and as an adjunctive agent to thrombolytic therapy in acute myocardial infarction. Ridogrel, a combined thromboxane synthase inhibitor, and receptor antagonist is used with streptokinase as an adjunctive therapy to reduce the formation and size of blood clots. Blood clots can cause ischemic cardiac events (heart attacks). Ridogrel has the dual property of inhibiting the synthesis of thromboxane and blocking the receptors of thromboxane/prostaglandin/endoperoxides. It has been shown to accelerate the speed of recanalization and to delay or prevent reocclusion during systemic thrombolysis with tissue plasminogen activator (streptokinase). Ridogrel is a more potent antiplatelet agent than aspirin and might offer an advantage over aspirin as an adjunct to thrombolysis in patients suffering from acute myocardial infarction. While aspirin inhibits cyclooxygenase, the enzyme responsible for producing thromboxane, ridogrel inhibits thromboxane synthesis directly. Ridogrel has been studied primarily as an adjunctive agent to thrombolytic therapy in acute MI (AMI). Despite positive results from initial pilot studies, the largest clinical study, the Ridogrel versus Aspirin Patency Trial (RAPT) failed to demonstrate any advantage with this agent over aspirin. In the study of 907 patients with AMI, there was no difference in the primary endpoint of infarct vessel patency rate between those randomized to ridogrel (72.2%) or aspirin (75.5%). Various mechanisms are likely responsible for the results seen with ridogrel in clinical trials, including potentially ineffective thromboxane receptor inhibition with the concentrations of ridogrel used in human studies. As such, there currently are no clinical indications for preferential use of ridogrel over aspirin.

BN-2629 (also known as SJG-136 and SG2000), a dimeric pyrrolobenzodiazepine that binds in the minor groove of DNA and produces G-G interstrand cross-links via reactive N(10)-C(11)/N(10')-C(ll') imine/carbinolamine moieties. This drug was investigated in phase II clinical trials in patients with epithelial ovarian, primary peritoneal, or fallopian tube cancer, however, these studied were terminated because of the slow accrual. In addition, BN-2629 participated in phase I/II trial in participants with advanced chronic lymphocytic leukemia and acute myeloid leukemia, but Spirogen also terminated these studies.

Apan (PPI-1019) is the lead compound of a series of β-amyloid-derived peptides designed by Praecis Pharmaceuticals in the US to interact with β-amyloid peptide, facilitating its clearance. Apan is derived from the D-enantiomeric Cholyl-LVFFA-NH2. Apan is developed by Praecis Pharmaceuticals to treat Alzheimer's Disease. Apan inhibits the aggregation of beta-amyloid and its associated nerve cell toxicity. In addition, Apan reaches the brain in quantities that are sufficient to block the aggregation of beta-amyloid molecules and alter the course of the disease. PPI-1019 completed phase I and II clinical trials and was found to be safe, well tolerated and amenable to cross bbb. After peptide administration, levels of Aβ1-40 in the CSF increased, which might be discussed as a sign for Aβ clearance out of the brain. PI-1019 had been in phase I/II clinical trials by Praecis Pharmaceuticals (acquired by GlaxoSmithKline in 2007) for the treatment of Alzheimer's disease(AD). However, this study had been discontinued.

Etiprednol dicloacetate (BNP-166; ethyl-17alpha-dichloroacetoxy-11beta-hydroxyandrosta-1,4-diene-3-one-17beta-carboxylate) is a new soft steroid. The compound proved to be a dissociated glucocorticoid, showing a reduction in transactivating activity while preserving transrepressive abilities. The compound effectively decreased cytokine production in lipopolysaccharide-stimulated lymphocytes and attenuated lectin-induced proliferation of blood mononuclear cells in tissue culture. The significant local effect of the compound will very likely be accompanied by a drastically reduced systemic activity indicating an encouraging selectivity of the pharmacological action of etiprednol dicloacetate. Etiprednol dicloacetate had been in a clinical trial for the treatment of allergic rhinitis, asthma and Crohn's disease. However, development has been discontinued.