Nickel (II) oxide is an olive gray powder, insoluble in water and soluble in acids. It is produced industrially and used mainly as an intermediate in the production of nickel alloys and as a hydrogenation catalyst. Long-term inhalation of NiO is damaging to the lungs, causing lesions and in some cases cancer.

Valdecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, is classified as a nonsteroidal anti-inflammatory drug (NSAID). Valdecoxib was manufactured and marketed under the brand name Bextra. Bextra was indicated for relief of the signs and symptoms of osteoarthritis and adult rheumatoid arthritis. For the treatment of primary dysmenorrhea. But in 2005 FDA requested that Pfizer withdraw Bextra from the American market, because the Agency had concluded that the overall risk versus benefit profile of Bextra was unfavorable. That conclusion was based on the potential increased risk for serious cardiovascular (CV) adverse events, an increased risk of serious skin reactions (e.g., toxic epidermal necrolysis, Stevens-Johnson syndrome, erythema multiforme) compared to other NSAIDs, and the fact that Bextra had not been shown to offer any unique advantages over the other available NSAIDs.

Gallium nitrate (brand name Ganite) is a drug that is used to treat hyper-calcemia, or too much calcium in the blood. Ganite exerts a hypocalcemic effect by inhibiting calcium resorption from bone, possibly by reducing increased bone turnover. It was shown, that gallium favorably altered the mineral properties to enhance hydroxyapatite crystallization and reduced mineral solubility. The drug also acted on the cellular components of bone to reduce bone resorption by decreasing acid secretion by osteoclasts. Nevertheless, ganite was withdrawn from sale, although the reasons was not the safety or effectiveness. Gallium nitrate inhibits the growth of various lymphoma cell lines in vitro and exhibits antitumor activity in patients with lymphoma. Gallium binds avidly to the iron transport protein transferrin. Transferrin-gallium complexes preferentially target cells that express transferrin receptors on their surface. Expression of transferrin receptors is particularly high on lymphoma cells. Cellular uptake of the gallium-transferrin complex leads to inhibition of cellular proliferation primarily via disruption of iron transport and homeostasis and blockade of ribonucleotide reductase. In phase II of clinical trials in patients with relapsed or refractory lymphoma, the antitumor activity of gallium nitrate is similar to, or better than, that of other commonly used chemotherapeutic agents.

Ritodrine (trade name Yutopar) is beta-2 adrenergic agonist used to stop premature labor. Ritodrine binds to beta-2 adrenergic receptors on the outer membrane of the myometrial cell, activates adenyl cyclase to increase the level of cAMP which decreases intracellular calcium and leads to a decrease of uterine contractions. In addition to stimulating the beta-2–adrenergic receptors of the uterine smooth muscle, ritodrine stimulates beta-adrenergic receptors of bronchial and vascular smooth muscles. The cardiostimulatory effects, including increased cardiac output, increased maternal and fetal heart rates, and widening of the maternal pulse pressure, are probably due to relaxation of the vascular smooth muscle. Relaxation of vascular smooth muscle stimulates the beta-1–adrenergic receptors and the reflex response to blood pressure. Also, during intravenous administration, ritodrine transiently increases maternal and fetal blood glucose and maternal plasma insulin concentrations. Other metabolic changes include increased cAMP, lactic acid, and free fatty acids, and decreased serum potassium concentration. Most side effects of β2 agonists result from their concurrent β1 activity and include the increase in heart rate, rise in systolic pressure, decrease in diastolic pressure, chest pain secondary to myocardial infarction, and arrhythmia. Beta-agonists may also cause fluid retention secondary to decrease in water clearance, which when added to the tachycardia and increased myocardial work, may result in heart failure. In addition, they increase gluconeogenesis in the liver and muscle resulting in hyperglycemia, which increases insulin requirements in diabetic patients. The passage of β agonists through the placenta does occur and may be responsible for fetal tachycardia, as well as hypoglycemia or hyperglycemia at birth.