Phosphocreatine (creatine phosphate, PCr, PC) is the phosphorylated form of endogenous creatine that serves as a rapidly mobilizable reserve of high-energy phosphates in skeletal muscle and the brain of vertebrates. Phosphocreatine is a key component in the intracellular system of energy buffering and transports from the site of energy production to the site of energy utilization to ensure that supply meets the high and dynamic demands of the heart. Phosphocreatine can anaerobically donate a phosphate group to ADP to form ATP during the first two to seven seconds following an intense muscular or neuronal effort. Conversely, excess ATP can be used during a period of low effort to convert creatine to phosphocreatine. The reversible phosphorylation of creatine is catalyzed by several creatine kinases. Particularly, PCr makes the energy of phosphoryl bonds of adenosine triphosphate (ATP) available at the myofibrillar creatine kinase that allows myocardium contraction. Supplementation with PCr was, therefore, suggested as potentially beneficial in patients with acute and chronic myocardial ischaemic injury. Phosphocreatine has been tried in the treatment of cardiac disorders and has been added to cardioplegic solutions. Phosphocreatine is used intravenously in hospitals in some parts of the world for cardiovascular problems under the name Neoton and also used by some professional athletes, as it is not a controlled substance.

Fonzine (also known as dimetotiazine) is an analgesics and anti-inflammatory agent marketed in Japan and Europe under the name Migristene and indicated for the treatment of migraine and headaches secondary to other disease. Fonzine exerts its activity by inhibiting serotonin and histamine H1 receptors.

Benzylthiouracil is a drug with anti-thyroid activity. It was developed for the treatment of multinodular goiter and hyperthyroidism. Benzylthiouracil treatment associated with severe adverse effects. It has been observed to be associated with antineutrophil cytoplasmic antibody-positive vasculitis, resulting in crescentic glomerulonephritis. Benzylthiouracil induced ANCA associated glomerulonephritis in patients with Graves' disease. Benzylthiouracil induces toxic hepatitis and lung damage.

Distigmine is an acetylcholinesterase (AChE) inhibitor. Distigmine shows direct binding to muscarinic receptors in the rat bladder, and repeated oral administration of distigmine causes downregulation of muscarinic receptors in the rat bladder. The observed direct interaction of distigmine with the bladder muscarinic receptors may partly contribute to the therapeutic and/or side effects seen in the treatment of detrusor underactivity. It is usually used to treat myasthenia gravis, dysuria due to hypotonic bladder such as neurogenic bladder or after surgery. Common side effects are: nausea/vomiting, abdominal pain, diarrhea, increased salivation, hypersecretion in respiratory tract, sweating, bradycardia, miosis, difficulty in breathing. Distigmine has a greater risk of causing cholinergic crisis because of accumulation of the drug being more likely than with neostigmine or pyridostigmine and so distigmine is rarely used as a treatment for myasthenia gravis, unlike pyridostigmine and neostigmine.

Trimebutine [3,4,5-trimethoxybenzoic acid 2-(dimethylamino)-2-phenylbutylester] is a noncompetitive spasmolytic agent. The actions of trimebutine on the gastrointestinal tract are mediated via (i) an agonist effect on peripheral mu, kappa and delta opiate receptors and (ii) release of gastrointestinal peptides such as motilin and modulation of the release of other peptides, including vasoactive intestinal peptide, gastrin and glucagon. Trimebutine attenuated colonic motility mainly through the inhibition of L-type Ca(2+) channels at higher concentrations, whereas, at lower concentrations, it depolarized membrane potentials by reducing BK(ca) currents, resulting in the enhancement of the muscle contractions.Trimebutine accelerates gastric emptying, induces premature phase III of the migrating motor complex in the intestine and modulates the contractile activity of the colon. It is indicated for the treatment and relief of symptoms associated with the irritable bowel syndrome (spastic colon); and in postoperative paralytic ileus in order to accelerate the resumption of the intestinal transit following abdominal surgery.

Pirprofen is a non-steroidal anti-inflammatory drug, related structurally to drugs such as ibuprofen, ketoprofen and naproxen. Pirprofen was introduced by Ciba-Geigy in 1982 as a treatment for rheumatic diseases. In 1990 due to adverse effects, including some cases of fatal liver toxicity the manufacturers decided to discontinue marketing it worldwide. Pirprofen proved to be useful in the management of both rheumatoid arthritis and osteoarthritis and as an analgesic. In doses of 600-800 mg/d, pirprofen has been found to be as effective as, but not superior to, aspirin 3.6 g/d in relieving the more common symptoms of rheumatoid arthritis. Pirprofen is as effective as, but not superior to, other available NSAIDs in terms of efficacy, tolerability, and incidence of adverse effects. The recommended dosage in osteoarthritis is 450-600 mg/d.

Nalfurafine, an opioid κ-selective agonist, has been officially approved for resistant pruritus in HD patients on the basis of a well-evidenced clinical trial in Japan. Nalfurafine hydrochloride is a potent and selective agonist for mouse, rat, guinea pig, and human κ-opioid receptors without significant activity on µ- and δ-opioid receptors. Nalfurafine hydrochloride (2.5 and 5 ug/day) has been proven to be safe and effective for the treatment of HD patients with uremic pruritus resistant to antihistamines.

Arbekacin is a broad-spectrum aminoglycoside used to treat methicillin-resistant Staphylococcus aureus (MRSA). Arbekacin has antibacterial activities against high-level gentamicin-resistant Enterococci, multidrug-resistant Pseudomonas aeruginosa, and Acinetobacter baumannii et al. In a cell-free system, habekacin (arbekacin) interfered with polypeptide synthesis, caused codon misreading, and inhibited translocation of N-acetylphenylalanyl-tRNA from the acceptor site to the donor site on ribosomes. Arbekacin bound to both 50S and 30S ribosomal subunits. Arbekacin has been approved as an injectable formulation in Japan since 1990, under the trade name Habekacin, for the treatment of patients with pneumonia and sepsis caused by MRSA. Meiji Seika Pharma is developing an inhaled aerosol formulation of arbekacin for the treatment of hospital-acquired bacterial pneumonia and ventilator-associated bacterial pneumonia. Nobelpharma is developing an intravenous formulation of arbekacin sulfate, known as nonsense readthrough compound or NPC 14, for the treatment of Duchenne muscular dystrophy.

Camylofin is an antimuscarinic. This medication is used as antispasmodic in biliary colic, renal and ureteric colic, dysmenorrhoea, peptic ulcer and chronic enterocolitis. It is used to treat stomach ache in infants and children. Camylofin should be the first choice and may be preferred over other drugs for cervical dilatation and acceleration of active phase of labor.

Subarachnoid haemorrhage (SAH) following cerebral aneurysm rupture or trauma can result in the induction of secondary ischaemic brain damage via a decrease in microvascular perfusion, a disruption of the blood-brain barrier and consequent vasogenic oedema, and the delayed spasm of the major cerebral arteries (i.e. vasospasm). It is increasingly apparent that oxygen radical-induced, iron-catalyzed lipid peroxidation (LP) within the subarachnoid blood and vascular wall plays a key role in the occurrence of these secondary events. Tirilazad mesylate, is a nonglucocorticoid, 21-aminosteroid, is a potent cytoprotective inhibitor of LP that works by a combination of radical scavenging and membrane stabilizing properties. It has been demonstrated to attenuate the acute and delayed vascular consequences of SAH and to protect the brain against ischaemic insults. Tirilazad mesylate has been proposed to treat acute ischaemic stroke. When tested on animal models, tirilazad protects brain tissue, and reduces brain damage. However, the drug fails to treat, and even worsens a stroke when studied on a human being.