Pathways

Baricitinib is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Baricitinib passes through the liver and is then excreted from the body mainly through the kidney.

Bamlanivimab, also known as LY-CoV555 or LY3819253, is a human IgG1K monoclonal antibody (mAb) against the SARS-CoV2 spike protein, called S. This drug was synthesized from the first blood samples of a patient who recovered from COVID-19 in the USA. This molecule is not approved by the FDA, but it is authorized under an Emergency Use Authorization (EUA) for the treatment of COVID-19 patients. X-ray crystallography and cryo-EM structural determination suggest that this molecule binds the receptor-binding domain (RBD) of the spike protein of CoV-19. This binding overlaps the ACE2 binding site. Bamlanivimab is available as an intravenous injection.

Bamipine is a first-generation piperidine H1-antihistamine. H1-antihistamines interfere with the agonist action of histamine at the H1 receptor and are administered to attenuate inflammatory process in order to treat conditions such as allergic rhinitis, allergic conjunctivitis, and urticaria. Reducing the activity of the NF-κB immune response transcription factor through the phospholipase C and the phosphatidylinositol (PIP2) signalling pathways also decreases antigen presentation and the expression of pro-inflammatory cytokines, cell adhesion molecules, and chemotactic factors. Furthermore, lowering calcium ion concentration leads to increased mast cell stability which reduces further histamine release. First-generation antihistamines readily cross the blood-brain barrier and cause sedation and other adverse central nervous system (CNS) effects (e.g. nervousness and insomnia). Second-generation antihistamines are more selective for H1-receptors of the peripheral nervous system (PNS) and do not cross the blood-brain barrier. Consequently, these newer drugs elicit fewer adverse drug reactions.

Balsalazide, brand name Colazal, is an aminosalicylate anti-inflammatory drug used in the treatment of mildly to moderately active ulcerative colitis. Balsalazide works by delivering its metabolite 9mesalazine) to the large intestine to act directly on ulcerative colitis. Mesalazine is also known as 5-aminosalicylic acid (5-ASA). Balsalazide disodium is delivered intact to the colon where it is cleaved by bacterial azoreduction. The mechanism of action of 5-aminosalicylic acid is unknown. Like the other NSAIDs, it probably targets the prostaglandin G/H synthase-1 (COX-1) and prostaglandin G/H synthase-2 (COX-2) in the cyclooxygenase pathway. The cyclooxygenase pathway begins in the cytosol with phospholipids being converted into arachidonic acid by the action of phospholipase A2. The rest of the pathway occurs on the endoplasmic reticulum membrane, where prostaglandin G/H synthase 1 & 2 convert arachidonic acid into prostaglandin H2. Prostaglandin H2 can either be converted into thromboxane A2 via thromboxane A synthase, prostacyclin/prostaglandin I2 via prostacyclin synthase, or prostaglandin E2 via prostaglandin E synthase. COX-2 is an inducible enzyme, and during inflammation, it is responsible for prostaglandin synthesis. It leads to the formation of prostaglandin E2 which is responsible for contributing to the inflammatory response by activating immune cells and for increasing pain sensation by acting on pain fibers. Salsalate inhibits the action of COX-1 and COX-2 on the endoplasmic reticulum membrane. This reduces the formation of prostaglandin H2 and therefore, prostaglandin E2 (PGE2). The low concentration of prostaglandin E2 attenuates the effect it has on stimulating immune cells and pain fibers, consequently reducing inflammation and pain. Moreover, it is possible that this drug also inhibits the lipoxygenase pathway (catalyzes the formation of leukotrienes and hydroxyeicosatetraenoic acids from arachidonic acid and its metabolites) by inhibiting the enzyme named arachidonate 5-lipoxygenase.