Norbolethone is a 19-nor anabolic steroid first synthesized in 1966. During the 1960s it was administered to humans in efficacy studies concerned with short stature and underweight conditions. It has never been reported by doping control laboratories prior to 2001. Norbolethone matches the description for what is described as a "designer steroid. " In fact, Norbolethone was given in clinical trials over 30 years ago and never given the green light. No supply was ever manufactured, and no test was ever developed to detect this substance, yet ironically, it was suspected of being used in the 2000 Olympics based on blood and urine assays done by the IOC. Norbolethone was used in the treatment of idiopathic underweight, prevention of indomethacin-induced intestinal ulcers.

Hafnium oxide is a radio enhancer; its nanoparticles (NBTXR3) were designed for high dose energy deposition within cancer cells when exposed to ionizing radiation. When activated by radiotherapy (RT), NBTXR3 allows for a higher energy deposit than RT alone, yielding an increased tumoral cell death. Nanocrystals of hafnium oxide are under investigation in phase II/III in patients with locally advanced soft tissue sarcoma (STS) of the extremity and trunk wall. In addition, NBTXR3, nanoparticles are being studied in phase I/II in patients with head and neck cancer; liver cancer; prostate cancer and rectal cancer.

Cloxypendyl is an antipsychotic drug, invented in the 1960s by the Deutsche Gold und Silber-Scheideanstalt vormals Roessler. The compound was 3.5 times more effective than chlorpromazine in the mouse catalepsy test. No clinical and commercial development was reported.

JNJ-37822681 is a novel, potent, specific, centrally active, dopamine D2 receptor antagonist, which was developed by Johnson & Johnson. This drug is in the phase II of clinical trial for the treatment of schizophrenia. JNJ-37822681 has optimal brain disposition and somnolence was the most frequently reported adverse effect.

JNJ-37822681 is a novel, potent, specific, centrally active, dopamine D2 receptor antagonist, which was developed by Johnson & Johnson. This drug is in the phase II of clinical trial for the treatment of schizophrenia. JNJ-37822681 has optimal brain disposition and somnolence was the most frequently reported adverse effect.

Avasimibe (CI 1011) is a potent ACAT (Acyl-CoA:cholesterol acyltransferase) inhibitor. Avasimibe inhibits both ACAT1 and ACAT2 isoforms. Avasimibe was in development by Parke-Davis (now Pfizer) in the US for the treatment of atherosclerosis and hyperlipidaemia. Avasimibe was in phase III studies and more than 1300 patients had been treated for up to one year, however, in October 2003, Pfizer announced that development had been discontinued.

SAR407899 is a potent, ATP-competitive Rho kinase inhibitor. It antihypertensive action in animals. Sanofi is developing SAR 407899 for the treatment of microvascular angina (Syndrome X). It was previously being developed in clinical trials for the treatment of diabetic neuropathies, diabetic nephropathies, erectile dysfunction, pulmonary hypertension, hypertension and kidney disorders, but development was discontinued for those indications.

Indium Chloride In-113 is a salt of the only stable Indium isotope with applications in organic synthesis as a Lewis acid. Indium Chloride is the most available soluble derivative of indium with high reproductive toxicity. In in vitro models, Indium Chloride inhibits cell viability by elevating intracellular ROS and inducing apoptosis. In animal models Indium chloride exposure cause the accumulation of indium in blood and lung, bone marrow micronucleus rate increased, the occurrence of oxidative damage and pathological changes. Besides that, the indium chloride exposed showed significant toxicity to sperm function, as well as an increased percentage of sperm morphological abnormality and chromatin DNA damage.

Mannose 6-phosphate (M6P) has type-I integral membrane receptors. M6P-receptors bind and transport M6P-enzymes to lysosomes, but it can also modulate the activity of a variety of extracellular M6P-glycoproteins (i.e., latent TGFbeta precursor, urokinase-type plasminogen activator receptor, Granzyme B, growth factors, Herpes virus). M6P has been demonstrated to reduce active TGF-β1 expression on cultured tendon fibroblasts and improved range of movement in a rabbit flexor tendon injury model. Studies of M6P in relation to skin scarring demonstrate improvement in scar cosmesis and accelerated return of normal dermal architecture. Juvidex, a formulation of M6P, inhibits the activation of TGF-beta1 and TGF-beta2, which are present at high levels in adult wounds that scar. On the other hands, M6P in a 600 mM hypertonic solution (Adaprev) potentially acts via a physical, non-chemical, hyperosmotic effect.