Browsing Pathways

Tiaprofenic Acid (also named tiaprofensaeure and surgam) is a nonsteroidal anti-inflammatory drug (NSAID). It can be used to treat pain (especially arthritic pain). Tiaprofenic can block prostaglandin synthesis by the action of inhibition of prostaglandin G/H synthase 1 and 2. Prostaglandin G/H synthase 1 and 2 catalyze the arachidonic acid to prostaglandin G2, and also catalyze prostaglandin G2 to prostaglandin H2 in the metabolism pathway. Decreased prostaglandin synthesis in many animal model's cell is caused by presence of tiaprofenic.

Tenoxicam (also named mobiflex and tilcotil) is a nonsteroidal anti-inflammatory drug (NSAID). It can be used to reduce inflammation, swelling, stiffness, and pain that are associated with various diseases such as tendinitis, bursitis and etc. Tenoxicam can block prostaglandin synthesis by the action of inhibition of prostaglandin G/H synthase 1 and 2. Prostaglandin G/H synthase 1 and 2 catalyze the arachidonic acid to prostaglandin G2, and also catalyze prostaglandin G2 to prostaglandin H2 in the metabolism pathway. Decreased prostaglandin synthesis in many animal model's cell is caused by presence of tenoxicam.

Salsalate (also named Salflex, Disalcid or Salsitab) is a nonsteroidal anti-inflammatory drug (NSAID). It can be used to treat pain, fever and inflammation. Salsalate can block prostaglandin synthesis by the action of inhibition of prostaglandin G/H synthase 1 and 2. Prostaglandin G/H synthase 1 and 2 catalyze the arachidonic acid to prostaglandin G2, and also catalyze prostaglandin G2 to prostaglandin H2 in the metabolism pathway. Decreased prostaglandin synthesis in many animal model's cell is caused by presence of salsalate.

Salicylate-sodium (also named salsonin or clin) is a nonsteroidal anti-inflammatory drug (NSAID). It can be used for relieving pain and reducing fever. Salicylate-sodium can block prostaglandin synthesis by the action of inhibition of prostaglandin G/H synthase 1 and 2. Prostaglandin G/H synthase 1 and 2 catalyze the arachidonic acid to prostaglandin G2, and also catalyze prostaglandin G2 to prostaglandin H2 in the metabolism pathway. Decreased prostaglandin synthesis in many animal model's cell is caused by presence of salicylate-sodium.

Salicylic acid (also named rutranex or salonil) is a nonsteroidal anti-inflammatory drug. Salicylic acid is also an important active metabolite of aspirin (acetylsalicylic acid). It can be used to reduce pain and fever. Salicylic acid can block prostaglandin synthesis by the action of inhibition of prostaglandin G/H synthase 1 and 2. Prostaglandin G/H synthase 1 and 2 catalyze the arachidonic acid to prostaglandin G2, and also catalyze prostaglandin G2 to prostaglandin H2 in the metabolism pathway. Decreased prostaglandin synthesis in many animal model's cell is caused by presence of Salicylic acid.

Acetaminophen (also named paracetamol or APAP) is not a Nonsteroidal anti-inflammatory drugs (NSAIDs). However, it still can be used to treat pain and fever. Acetaminophen can block prostaglandin synthesis by the action of inhibition of prostaglandin G/H synthase 1 and 2. Prostaglandin G/H synthase 1 and 2 catalyze the arachidonic acid to prostaglandin G2, and also catalyze prostaglandin G2 to prostaglandin H2 in the metabolism pathway. Decreased prostaglandin synthesis in many animal model's cell is caused by presence of acetaminophen.

Tobramycin (also named aktob or tobi) is an aminoglycoside antibiotic that can be used to treat various gram-negative bacterial infections such as the species of Pseudomonas. Bacterial 30S ribosomal subunit protein and four nucleotides of 16S rRNA will be bound with tobramycin irreversibly to cause misreading of mRNA; so that formation of mRNA could be prevented because of incorrect insertion of amino acids to polypeptide will result nonfunctional or toxic peptides. Therefore, there is no protein synthesis for bacteria.

Tigecycline is a glycylcycline, a class of antibiotics derived from tetracycline. Tigecycline has broad spectrum antibacterial abilities and is not susceptible to traditional tetracycline resistance mechanisms such as ribosomal protection and efflux by tetracycline-specific pumps. Tigecycline inhibits bacterial protein synthesis by binding to the A site of the 16s rRNA on the 30S ribosomal subunit. By binding to the A site, tigecycline prevents tRNA from docking onto the 16S rRNA with it’s codon ultimately halting the addition of amino acids to elongate peptide chains used in protein structures.

Arbekacin, trade name Habekacin, is an aminoglycoside antibiotic derived from dibekacin that inhibits bacterial protein synthesis. Arbekacin is prescribed to patients with sepsis and pneumonia resulting from MRSA. Arbekacin binds the bacterial 50S and 30S ribosomal subunit proteins and prevents the formation of the initiation complex with messenger RNA. More specifically, Arbekacin binds four nucleotides of the 16S rRNA and a single amino acid of protein S12. This interferes with the decoding site in the vicinity of nucleotide 1400 in 16S rRNA of the 30S subunit. This region interacts with the wobble base of the anticodon of tRNA. This causes interference of the initiation complex, misreading of mRNA so that incorrect amino acids are inserted into the polypeptide leading to nonfunctional or toxic peptides, and the breakup of polysomes into nonfunctional monosomes. Arbekacin is effective at treating Gram-positive bacteria like Staphylococcus aureus and Staphylococcus epidermidis and Gram-negative bacteria such as Pseudomonas aeruginosa.

Paromomycin (also known as Aminosidin) is an antimicrobial that can be used for treatment of various parasitic infections. By binding to the A site of ribosomal RNA complexes, paramomycin can lead to production of incorrect polypeptide chain in bacteria, which cause incorrect protein production and eventually, the death of bacteria. Therefore, paramomycin can kill bacteria by inhibiting their protein synthesis that lead to bacterial death.