Valproic acid (VPA; valproate; di-n-propylacetic acid, DPA; 2-propylpentanoic acid, or 2-propylvaleric acid) was first synthesized in 1882, by Burton. FDA approved valproic acid for the treatment of manic episodes associated with bipolar disorder, for the monotherapy and adjunctive therapy of complex partial seizures and simple and complex absence seizures and adjunctive therapy in patients with multiple seizure types that include absence seizures and for the prophylaxis of migraine headaches. The mechanisms of VPA which seem to be of clinical importance in the treatment of epilepsy include increased gamma-aminobutyric acid (GABA)-ergic activity, reduction in excitatory neurotransmission, and modification of monoamines. Recently, it was discovered that the VPA is a class I selective histone deacetylase inhibitor. This activity can be distinguished from its therapeutically exploited antiepileptic activity.

Pralidoxime is a cholinesterase reactivator used as the antidote to organophosphate pesticides or acetylcholinesterase inhibitors (nerve agents) in conjunction with atropine and diazepam. Organophosphates bind to the esteratic site of acetylcholinesterase, which results initially in reversible inactivation of the enzyme. Acetylcholinesterase inhibition causes acetylcholine to accumulate in synapses, producing continuous stimulation of cholinergic fibers throughout the nervous systems. If given within 24 hours after organophosphate exposure, pralidoxime reactivates the acetylcholinesterase by cleaving the phosphate-ester bond formed between the organophosphate and acetylcholinesterase. Pralidoxime is indicated as an adjunct in the treatment of moderate and severe poisoning caused by organophosphate pesticides that have anticholinesterase activity or by chemicals with anticholinesterase activity such as some chemicals used as nerve agents during chemical warfare. Pralidoxime is also indicated as an adjunct in the management of the overdose of cholinesterase inhibitors, such as ambenonium, neostigmine, and pyridostigmine, used in the treatment of myasthenia gravis. Pralidoxime, used in conjunction with atropine, reverses nicotinic effects, such as muscle weakness and fasciculation, respiratory depression, and central nervous system (CNS) effects, associated with toxic exposure to organophosphate anticholinesterase pesticides and chemicals and with cholinesterase inhibitor overdose. Atropine, by antagonizing the action of cholinesterase inhibitors at muscarinic receptor sites, reverses muscarinic effects, such as tracheobronchial and salivary secretion, bronchoconstriction, bradycardia, and, to a moderate extent, CNS effects.

Vincristine is a vinca alkaloid antineoplastic agent used as a treatment for various cancers including breast cancer, Hodgkin's disease, Kaposi's sarcoma, and testicular cancer. The vinca alkaloids are structurally similar compounds comprised of 2 multiringed units, vindoline and catharanthine. The vinca alkaloids have become clinically useful since the discovery of their antitumour properties in 1959. Initially, extracts of the periwinkle plant (Catharanthus roseus) were investigated because of putative hypoglycemic properties, but were noted to cause marrow suppression in rats and antileukemic effects in vitro. Vincristine binds to the microtubular proteins of the mitotic spindle, leading to crystallization of the microtubule and mitotic arrest or cell death. Vincristine has some immunosuppressant effect. The vinca alkaloids are considered to be cell cycle phase-specific. The antitumor activity of Vincristine is thought to be due primarily to inhibition of mitosis at metaphase through its interaction with tubulin. Like other vinca alkaloids, Vincristine may also interfere with: 1) amino acid, cyclic AMP, and glutathione metabolism, 2) calmodulin-dependent Ca2+-transport ATPase activity, 3) cellular respiration, and 4) nucleic acid and lipid biosynthesis.Vincristine was marketed under the brand name Oncovin, but was discontinued. In 2012 the FDA approved a Liposomal formulation of Vincristine, named MARQIBO KIT.

Acetylcysteine (also known as N-acetylcysteine or N-acetyl-L-cysteine or NAC) is primarily used as a mucolytic agent and in the management of acetaminophen poisoning. Acetylcysteine likely protects the liver by maintaining or restoring the glutathione levels, or by acting as an alternate substrate for conjugation with, and thus detoxification of, the reactive metabolite. Nacystelyn (NAL), a recently-developed lysine salt of N-acetylcysteine (NAC) is known to have excellent mucolytic capabilities and is used to treat cystic fibrosis (CF) lung disease. NAC as a precursor to the antioxidant glutathione modulates glutamatergic, neurotrophic, and inflammatory pathways. The potential applications of NAC to facilitate recovery after traumatic brain injury, cerebral ischemia, and in treatment of cerebrovascular vasospasm after subarachnoid hemorrhage. Acetylcysteine serves as a prodrug to L-cysteine, which is a precursor to the biologic antioxidant, glutathione, and hence administration of acetylcysteine replenishes glutathione stores. L-cysteine also serves as a precursor to cystine, which in turn serves as a substrate for the cystine-glutamate antiporter on astrocytes hence increasing glutamate release into the extracellular space. Acetylcysteine also possesses some anti-inflammatory effects possibly via inhibiting NF-κB through redox activation of the nuclear factor kappa kinases thereby modulating cytokine synthesis. NAC is associated with reduced levels of inflammatory cytokines and acts as a substrate for glutathione synthesis. These actions are believed to converge upon mechanisms promoting cell survival and growth factor synthesis, leading to increased neurite sprouting.

Benzphetamine is a sympathomimetic agent with properties similar to dextroamphetamine. It is used in the management of exogenous obesity as a short term (a few weeks) adjunct in a regimen of weight reduction based on caloric restriction in patients with an initial body mass index (BMI) of 30 kg/m2 or higher who have not responded to appropriate weight reducing regimen (diet and/or exercise) alone. Presumably, benzphetamine produces its effects through mechanisms similar to amphetamine via induces synaptic vesicular amine transporter, but precise mechanism of action of benzphetamine is not known.

Chlorthalidone is a diuretic that is used for the treatment of hypertansion and edema. The drug is approved by FDA and either prescribed alone (Chlorthalidone trade name) or in combination with atenolol (Tenoretic trade name), azilsartan kamedoxomil (Edarbyclor) and clonidin (Clorpres). The mechanism of action is associated with activation of sodium and chloride renal excretion.

Chlorzoxazone is a centrally acting central muscle relaxant with sedative properties. It is claimed to inhibit muscle spasm by exerting an effect primarily at the level of the spinal cord and subcortical areas of the brain where it inhibits multisynaptic reflex arcs involved in producing and maintaining skeletal muscle spasm of varied etiology. The clinical result is a reduction of the skeletal muscle spasm with relief of pain and increased mobility of the involved muscles. Chlorzoxazone is indicated as an adjunct to rest, physical therapy, and other measures for the relief of discomfort associated with acute, painful musculoskeletal conditions. The mode of action of this drug has not been clearly identified, but may be related to its sedative properties. Chlorzoxazone does not directly relax tense skeletal muscles in man.

Meprobamate is a carbamate derivative used as an anxiolytic drug. Meprobamate enhances GABA-A currents, and at higher concentration, exhibits a separate channel-blocking effect that limits the magnitude of GABA(A) receptor potentiation. It is also a potent adenosine reuptake inhibitor (AdoRI), which is most likely responsible for its lesser degree of sedation compared to barbiturates. Meprobamate was withdrawn from European and Canadian markets due to its potential to cause physical and psychological dependence.

Leucovorin is a compound similar to folic acid, which is a necessary vitamin. It has been around and in use for many decades. Leucovorin is a medication frequently used in combination with the chemotherapy drugs fluoruracil and methotrexate. Leucovorin is not a chemotherapy drug itself, however it is used in addition to these chemotherapy drugs to enhance anticancer effects (with fluorouracil) or to help prevent or lessen side effects (with methotrexate). Leucovorin is also used by itself to treat certain anemia problems when folic acid deficiency is present.

Sodium tetradecyl sulfate is an anionic surfactant which occurs as a white, waxy solid. Sodium tetradecyl sulfate is the active component of the sclerosant drug Sotradecol. Sotradecol (sodium tetradecyl sulfate injection) is a sclerosing agent. Intravenous injection causes intima inflammation and thrombus formation. This usually occludes the injected vein. Subsequent formation of fibrous tissue results in partial or complete vein obliteration that may or may not be permanent. Sotradecol® (sodium tetradecyl sulfate injection) is indicated in the treatment of small uncomplicated varicose veins of the lower extremities that show simple dilation with competent valves. The benefit-to-risk ratio should be considered in selected patients who are great surgical risks. Sodium tetradecyl sulfate is a potent toxin for endothelial cells in that brief exposure to even low concentrations are effective in stripping endothelium over a considerable distance and exposing highly thrombogenic endothelium in the process. Diluted sodium tetradecyl sulfate is also able to induce a hypercoagulable state, possibly by selective inhibition of protein C, and can also promote platelet aggregation. In the UK, Ireland, Italy, Australia, New Zealand and South Africa, it is sold under the trade-name Fibro-Vein in concentrations of 0.2%, 0.5%, 1.0%, and 3%