Pathways

Alvimopan, also known as Entereg, is an opioid antagonist used to reduce the healing time of the upper and lower GI tract following surgical procedures. It is a μ-opioid antagonist action only on the peripheral receptors and not on the one in the central nervous system. Alvimopan competitively binds to the mu-opioid receptors in the GI tract, alvimopan owes its selectivity for peripheral receptors to its pharmacokinetics. The drug acts in the gastrointestinal tract by competing to bind the mu-opioid receptor. Alvimopan differs from other peripherally acting mu-receptor antagonists such as methylnaltrexone due to only acting on peripheral opioid receptors. It is used to permit a faster recovery of patients after surgical procedures that slow the GI tract transit (postoperative ileus). This drug is administered as an oral capsule. Alvimopan inhibits the mu-opioid receptor located on neurons in the intestine. This inhibits the exchange of GTP for GDP which is required to activate the G-protein complex. This prevents the Gi subunit of the mu opioid receptor from inhibiting adenylate cyclase, which can therefore continue to catalyze ATP into cAMP. cAMP increases the excitability in spinal cord pain transmission neurons which allows the patient to feel pain rather than the analgesic effects of opioids. The inhibition of Mu-type opioid receptors also prevents the Gi subunit of the mu opioid receptor from activating the inwardly rectifying potassium channel increasing K+ conductance which would cause hyperpolarization. Alvimopan also prevents the gamma subunit of the mu opioid receptor from inhibiting the N-type calcium channels on the neuron. This allows calcium to enter the neuron and depolarize. The inhibition of mu-opioid receptors prevents hyperpolarization in the neuron, allowing it to fire at a normal rate. The neuron is able to depolarize and the high concentration of calcium releases acetylcholine and nitric acid into the neuromuscular junction. Acetylcholine binds to nicotinic acetylcholine receptors on the smooth muscles of the intestines, causing muscle contraction. The nitric oxide diffuses into the myocyte and causes muscle relaxation. The rythmic action of the neurotransmitters creates the peristalsis and the good GI transit.

Amantadine is an antiviral used in the symptomatic treatment of various strains of influenza A virus. It can also be used to treat parkinsonism and drug-induced extrapyramidal reactions. The mechanism of action in the Parkinson's treatment is not known. As an antiviral, Amantadine interacts with the M2 (matrix protein 2) viral protein. This viral protein is an ion channel needed for the viral particule to become uncoated once it is in the host cells. This drug is available as an oral capsule and as a syrup,

Amantadine is a medication used to treat dyskinesia in Parkinson's patients who are recieving levodopa. It is also an antiviral medicine that is used to treat influenza A. The antiarkinsonic effects are not fully understood, but it appears to release dopamine from the nerve endings of brain cells as well as its NMDA receptor antagonistic effects. Amantadine is diffused across the blood-brain barrier after being absorbed from the intestine. It then antagonizes the NMDA receptor on the postsynaptic neurons in the brain which causes those neurons to hyperpolarize and prevents depolarization. The exact antiparkinsonic effects of this are unknown.

Ambenonium is a cholinesterase inhibitor used in the treatment of myasthenia gravis, helping to alleviate muscle weakness by stimulating muscle contraction and stimulation. Its mechanism of action is through reversible inhibition of acetylcholinesterase, this stops the breakdown of acetylcholine in the neuromuscular junction, allowing it to further interact with nicotinic receptors. Acetylcholine stimulates the nicotinic acetylcholine receptors and causes a cascade resulting in muscle contraction. As myasthenia gravis inhibits acetylcholine signal transmission by producing antibodies that bind to the receptors instead, stopping all signal transmission to initiate a muscle contraction. Ambenonium allows acetylcholine to be present in the neuromuscular junction for longer and increases the chances of signal transmission.

Ambenonium is a cholinesterase inhibitor used in the treatment of myasthenia gravis, helping to alleviate muscle weakness by stimulating muscle contraction and stimulation. Its mechanism of action is through reversible inhibition of acetylcholinesterase, this stops the breakdown of acetylcholine in the neuromuscular junction, allowing it to further interact with nicotinic receptors. Acetylcholine stimulates the nicotinic acetylcholine receptors and causes a cascade resulting in muscle contraction. As myasthenia gravis inhibits acetylcholine signal transmission by producing antibodies that bind to the receptors instead, stopping all signal transmission to initiate a muscle contraction. Ambenonium allows acetylcholine to be present in the neuromuscular junction for longer and increases the chances of signal transmission.

Metabolites of Ambrisentan are predicted with biotransformer.