Apramycin is a broad-spectrum aminocyclitol antibiotic produced by a strain of Streptomyces tenebrarius. It has a bactericidal action against many gram-negative bacteria. Apramycin is a structurally unique antibiotic that contains a bicyclic sugar moiety and a monosubstituted deoxystreptamine. It is not approved for use in humans. Apramycin is registered for use in more than twenty countries in cattle, pigs and chickens. The drug exerts its antibacterial effect by inhibiting protein synthesis at the level of peptidyl translocation. It is mostly used for treating gastrointestinal infections. Apramycin is available in soluble powder and feed premix formulations.

Romurtide (Muroctasin) is a non-specific immune stimulant derived from muramyl dipeptide, which is obtained from gram-positive bacterial cell walls. Muroctasin stimulates macrophages, which release interleukin-l, which in turn increases production of colony-stimulating factors; muroctasin also evokes an increased production of neutrophils. It is used in Japan for chemotherapy-induced leukopenia.

Tropisetron (Tropisetron-AFT) is a potent and selective serotonin 3 (5-hydroxytryptamine3; 5-HT3) receptor antagonist with antiemetic properties, probably mediated via antagonism of receptors both at peripheral sites and in the central nervous system. Surgery and treatment with certain substances, including some chemotherapeutic agents, may trigger the release of serotonin from enterochromaffin-like cells in the visceral mucosa and initiate the emesis reflex and its accompanying feeling of nausea. Tropisetron (Tropisetron-AFT) selectively blocks the excitation of the presynaptic 5-HT3 receptors of the peripheral neurons in this reflex, and may exert additional direct actions within the CNS on 5-HT3 receptors mediating the actions of vagal input to the area postrema.

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.