Histidine is an essential amino acid. L-histidine is converted to histamine by histidine decarboxylase, a pyridoxal 5'-phosphate-dependent enzyme. The copper(II)–l-histidine (1:2 complex at physiological pH) has been widely used in the treatment of Menkes disease (a genetic neurodegenerative disorder that leads to early death in the children due to impaired copper metabolism) and more recent use has been reported in the treatment of infantile hypertrophic cardioencephalomyopathy (a condition caused by mutations in SCO2, a cytochrome c oxidase assembly gene). CUSTODIOL HTK (Histidine-tryptophan-ketoglutarate) Solution is indicated for perfusion and flushing of donor kidneys, liver, and heart prior to removal from the donor or immediately after removal from the donor.

Nandrolone, also known as 19-nortestosterone or 19-norandrostenolone, is a semisynthetic anabolic-androgenic steroid derived from testosterone. Nandrolone is used in the form of a variety of long-acting prodrug esters for intramuscular injection, the most common of which are nandrolone decanoate. Nandrolone decanoate is indicated for the management of the anemia of renal insufficiency and has been shown to increase hemoglobin and red cell mass. Certain clinical effects and adverse reactions demonstrate the androgenic properties of this class of drugs. Complete dissociation of anabolic and androgenic effects has not been achieved. The actions of anabolic steroids are therefore similar to those of male sex hormones with the possibility of causing serious disturbances of growth and sexual development if given to young children. Anabolic steroids suppress the gonadotropic functions of the pituitary and may exert a direct effect upon the testis. Anabolic steroids have been reported to increase low-density lipoproteins and decrease high-density lipoproteins. Synthetic version of nandrolone was developed in 1950. But nandrolone for sale appeared later only in 1962 in the form of decanoate under the trade name Deca-Durabolin (Organon company).

Pittsburgh compound B (PiB) is a radioactive analog of thioflavin T, which can be used in positron emission tomography scans to image beta-amyloid plaques in the brains of patients with Alzheimer’s disease. 11C-PIB specifically binds to Aβ40 and Aβ42 fibrils and insoluble plaques containing the aforementioned Aß peptides with no detectable binding to soluble Aβ forms or neurofibrillary tangles under PET study conditions. Furthermore, this radiotracer does not bind to neurofibrillary tangles (NFTs) in the neuronal regions of the brain during postmortem autopsies. A typical injected dose ranges from 250-450 MBq and the imaging time normally varies between 40 and 90 minutes. The quantification of 11C-PIB has demonstrated to elicit a profound difference in neuronal cortical binding between individuals recognized with Alzheimer's disease and age-matched cognitively normal controls.

Verteporfin (trade name Visudyne), a benzoporphyrin derivative, is a medication used for the treatment of patients with predominantly classic subfoveal choroidal neovascularization due to age-related macular degeneration, pathologic myopia or presumed ocular histoplasmosis syndrome. Verteporfin can also be used to destroy tumors. Verteporfin is a 1:1 mixture of two regioisomers (I and II), VISUDYNE therapy is a two-stage process requiring administration of both verteporfin for injection and nonthermal red light. Verteporfin accumulates in these abnormal blood vessels and, when stimulated by nonthermal red light with a wavelength of 689 nm in the presence of oxygen, produces highly reactive short-lived singlet oxygen and other reactive oxygen radicals, resulting in local damage to the endothelium and blockage of the vessels. Verteporfin is also used off-label for the treatment of central serous retinopathy. Verteporfin is given intravenously, 15 minutes before laser treatment. Light activation of verteporfin results in local damage to neovascular endothelium, resulting in vessel occlusion. Damaged endothelium is known to release procoagulant and vasoactive factors through the lipo-oxygenase (leukotriene) and cyclo-oxygenase (eicosanoids such as thromboxane) pathways, resulting in platelet aggregation, fibrin clot formation and vasoconstriction. Verteporfin appears to somewhat preferentially accumulate in neovasculature, including choroidal neovasculature. However, animal models indicate that the drug is also present in the retina. Therefore, there may be collateral damage to retinal structures following photoactivation including the retinal pigmented epithelium and outer nuclear layer of the retina. The temporary occlusion of choroidal neovascularization (CNV) following VISUDYNE therapy has been confirmed in humans by fluorescein angiography.

Mivacurium chloride (Mivacron) is a new benzylisoquinolinium choline-like diester neuromuscular blocking drug with an onset of action at equipotent doses that is comparable to atracurium and vecuronium but slower than succinylcholine. MIVACRON (a mixture of three stereoisomers) binds competitively to cholinergic receptors on the motor end-plate to antagonize the action of acetylcholine, resulting in a block of neuromuscular transmission. This action is antagonized by acetylcholinesterase inhibitors, such as neostigmine. MIVACRON is a short-acting neuromuscular blocking agent indicated for inpatients and outpatients, as an adjunct to general anesthesia, to facilitate tracheal intubation and to provide skeletal muscle relaxation during surgery or mechanical ventilation.