Cefminox is a broad-spectrum, bactericidal cephalosporin antibiotic. It is especially effective against Gram-negative and anaerobic bacteria. It is indicated in treatment of the following infections caused by sensitive bacteria: 1. Respiratory infections: Amygdalitis, circumtonsillar abscess, bronchitis, bronchiolitis, bronchiectasis (in fection), secondary infections of chronic respiratory diseases, pneumonia, and pulmonary suppuration; 2. Infection in urinary system: Nephropyelitis, cystitis; 3. Infections in abdominal cavity: Cholecystitis' angiocholitis'peritonitis; 4. Infections in pelvic cavity: Pelvic peritonitis, adnexitis, intrauterine infection, inflammation in pelvic dead space, and parametritis; 5. Septicaemia.

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.

Clonixin is a nonsteroidal agent. It is an anilino-nicotinic acid derivative. It is a drug of anti-inflammatory antipyretic and analgesic activity that produces minor digestive side-effects. At high concentrations, clonixin inhibited PGE2 formed by COX-2 and partly by COX-1 activity. The drug is indicated for the relief of headaches, muscle aches, joint, dental, ear, dysmenorrhea, post-traumatic, post-surgical, gynecological. Adverse effects are occasionally nausea, dizziness, and somnolence, were mild and transient. On rare occasions, and administering high doses, it is possible the appearance of dry mouth or constipation. Concomitant use of anticholinergic drugs to be avoided by the possibility that they enhance their effects atropine.

Cefazedone is a semisynthetic first-generation cephalosporin with activity against Gram-positive and Gram-negative bacteria. Cefazedone binds to and inactivates penicillin-binding proteins (PBPs) located on the inner membrane of the bacterial cell wall. PBPs are enzymes involved in the terminal stages of assembling the bacterial cell wall and in reshaping the cell wall during growth and division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis. Unlike other cephalosporins cefazedone possesses good activity against gram-positive bacteria

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.

Bendazac, (1-benzyl-1H-indazol-3-yl-oxy)-acetic acid, is structurally related to indomethacin. Its lysine salt has been reported to be absorbed better than the parent compound. It is applied topically as bendazac lysine 0.5% (wt/vol) aqueous solution for delaying the progression of cataract. Topical application of bendazac is associated with transient burning sensation. It reduces the secretion of the skin ulcer surface, promotes skin formation and accelerates tissue repair.

Azidocillin is a narrow-spectrum, semisynthetic penicillin derivative with antibacterial activity towards Grain-positive and Gram-negative microorganisms, including Haemophilus influenze, against which it is as effective as ampicillin. Azidocillin binds to and inactivates penicillin-binding proteins (PBPs) located on the inner membrane of the bacterial cell wall. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This interrupts bacterial cell wall synthesis and results in the weakening of the bacterial cell wall, eventually causing cell lysis. Azidocillin can be applied in the treatment of inflammation of upper airways, middle ear, sinuses, throat, larynx and palatine tonsils. The substance is excreted with urine in 50-70% in the unchan¬ged form. It binds to the blood plasma proteins in 84%, and its half-life period is 30 min. The side effects are similar as those of benzylpenicillin but occur less frequently.

Fendiline or Sensit (N-(3,3-diphenylpropyl)-(1-phenylethyl)-amine), is a diphenylalkylamine blocker of L-type calcium channels. Fendiline is an anti-anginal agent for the treatment of coronary heart disease. Pharmaco-dynamically, it exerts the typical calcium as well as calmodulin antagonistic actions: inhibition of the transmembrane calcium current, smooth muscle relaxation, negative inotropism, cardioprotection, inhibition of calmodulin-activated myosin light-chain kinase and phosphodiesterase. Pharmacokinetics reveal slow onset of action and a long half-life. The anti-anginal and anti-ischaemic efficacy of fendiline has been proven in several placebo-controlled, double-blind trials. Fendiline is an FDA-approved, albeit now clinically obsolete. Additionally, fendiline is a specific inhibitor of K-Ras plasma membrane localization that also inhibits K-Ras signal output and blocks the proliferation of K-Ras-transformed tumor cells.

Masitinib is a new orally administered tyrosine kinase inhibitor that targets mast cells and macrophages, important cells for immunity, through inhibiting a limited number of kinases. Based on its unique mechanism of action, masitinib can be developed in a large number of conditions in oncology, in inflammatory diseases, and in certain diseases of the central nervous system. In oncology due to its immunotherapy effect, masitinib can have an effect on survival, alone or in combination with chemotherapy. Through its activity on mast cells and consequently the inhibition of the activation of the inflammatory process, masitinib can have an effect on the symptoms associated with some inflammatory and central nervous system diseases and the degeneration of these diseases. AB Science is developing masitinib in multiple sclerosis and alzheimer's disease. Masitinib targets kinases, including c-Kit, PDGFR, and Lyn. It is used in the treatment of mast cell tumors in animals, specifically dogs. Since its introduction in November 2008 it has been distributed under the commercial name Masivet. It has been available in Europe since the second part of 2009. In the USA it is distributed under the name Kinavet.

Tilarginine is L-N-monomethyl arginine (L -NMMA), a non-selective inhibitor of nitric oxide synthase (NOS), which has been studied in the treatment of septic shock and cardiogenic shock complicating myocardial infarction. Despite strong evidence that excessive nitric oxide (NO) production plays a pivotal role in the pathogenesis of septic shock and may contribute to the pathogenesis of cardiogenic shock complicating myocardial infarction, outcome studies in these two disorders have proved disappointing. Tilarginine therapy was associated with an excess mortality, particularly at doses > 5 mg/(kg h), in septic shock, whereas the effects of a lower dose (1 mg/(kg h)) in cardiogenic shock complicating myocardial infarction were neutral. The excess mortality in patients with septic shock was almost certainly the result of unfavorable hemodynamic changes induced by Tilarginine (decreased cardiac output, increased pulmonary vascular resistance and reduced tissue oxygen delivery) whereas the lack of benefit in patients with cardiogenic shock complicating myocardial infarction may have been because the dose of Tilarginine was too low.