Cinamolol is cinnamic acid derivative with adrenergic β-receptor blocking activity developed by Lyonnaise Industrielle Pharmaceutique

IPROCROLOL is a beta-adrenoceptor antagonist with antiarrhythmic properties.

Cefrotil is an antibiotic drug patented by pharmaceutical company Farbwerke Hoechst A.-G. And used as pharmaceutical intermediates

Cefaloram is aminocephalosporanic acid derivative with potent antibacterial activity. Cefaloram 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

Procinolol is phenoxypropanol derivative patented by Societe Industrielle pour la Fabrication des Antibiotiques for treating angina and cardiac rhythm disorders

Pargolol (also Kö 1400) is a beta-adrenergic receptor blocking agent that was developed as an antiarrhythmic agent. However, information about the further development of this drug is not available.

Pirazmonam is a potent anti-gram-negative monobactam that is differentiated from aztreonam by its high intrinsic activity against Ps. aeruginosa and good activity against Pseudomonas species. Pirazmonam has generally poor activity against gram-positive aerobic bacteria and anaerobic bacteria. Pirazmonam is a Trojan Horse molecule containing a b-lactam antibiotic that has been developed based on bacterial iron uptake systems. It features high structural similarity to aztreonam attached to a 3-hydroxy-4-pyridinone iron chelating group. Pirazmonam exhibited strong affinity to penicillin-binding protein 3 (PBP3) of Escherichia coli and moderate to negligible affinity to the other E. coli PBPs.

Quinacillin is semisynthetic penicillase-resistant penicillin patented by Boots Pure Drug Co. Ltd. For the treatment of bacterial infection. Quinacillin 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. In clinical trials Staph. aureus was eradicated from all but two patients during treatment but recurred in 4 after withdrawal. The antibiotic was especially useful in the treatment of staphylococcal respiratory infections, as it has little effect on the normal bacterial flora of the chest.

Picumeterol (GR114297A) is a potent and highly selective beta2-adrenoceptor agonist with a longer duration of action than salbutamol, but shorter than salmeterol. Picumeterol is the (R)-isomer of the racemic entity GR63411B, and picumeterol has been shown to be about 40 times more potent than the (S)-isomer (GR114744A) in various in vitro pharmacological models of beta2-agonist activity. Picumeterol is of potential value in the treatment of asthma and related diseases in man following inhalation administration. In the clinical studies, the bronchodilator potencies of picumeterol and GR 63411B were similar. However, both drugs were short-acting, which is at odds with their activity in vitro. These compounds display dissociation between bronchodilator activity and protection against methacholine-induced bronchoconstriction.

Cefuroxime Pivoxetil is an ester prodrug of cefuroxime, a semisynthetic, broad-spectrum, beta-lactamase-resistant, second-generation cephalosporin with antibacterial activity. Cefuroxime 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.